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PubMed1995

Acoustic propagation properties of normal, stunned, and infarcted myocardium. Morphological and biochemical determinants.

BACKGROUND: Identification of viable but stunned myocardium remains a major problem. Since stunned myocardium results in impairment of myocardial function without any structural damage and infarcted myocardium causes major structural disruption, we postulated that acoustic properties could distinguish between the two insults. METHODS AND RESULTS: Anesthetized open-chest dogs underwent a total occlusion of the left anterior descending coronary artery for 15 minutes (stunned, n = 7) and 90 minutes (infarcted, n = 8), followed by reperfusion for 3 hours. Circumflex coronary artery perfusion territory (n = 15) served as normal control tissue. Regions of myocardium were quantitatively evaluated with a scanning laser acoustic microscope operating at 100 MHz and a research ultrasound system operating at 4 to 7 MHz. Four ultrasonic parameters were determined: attenuation coefficient (an index of loss per unit distance), speed of propagation, a spatial variation of propagation speed called the heterogeneity index (HI), and ultrasonic backscatter at 5 MHz (IBR5). Myocardial water, lipid, and protein contents of normal, stunned, and infarcted myocardium were also determined. The attenuation coefficient of normal myocardium (179 +/- 20 dB/cm) was significantly greater than that of stunned (136 +/- 7 dB/cm, P < .001) and infarcted (130 +/- 8 dB/cm, P < .001) myocardium. The propagation speed of normal myocardium (1597 +/- 6 m/s) was similar to that of stunned (1600 +/- 6 m/s) and significantly higher than that of infarcted (1575 +/- 7 m/s, P < .001) myocardium. The HI for specimen thicknesses of 75 to 100 microns showed an increase of 33% between normal (5.0 +/- 0.8 m/s) and stunned (7.5 +/- 2.3 m/s, P < .05) myocardium. However, for the infarcted myocardium (5.8 +/- 2.0 m/s), the HI was essentially the same as that of the normal myocardium (5.0 +/- 0.8 m/s). The IBR5 of normal (-47.1 +/- 1.0 dB) was not significantly different from that of stunned myocardium (-46.8 +/- 0.9 dB). The IBR5 of infarcted myocardium (-42.4 +/- 1.0 dB) was significantly greater than that of normal myocardium. Myocardial water and protein contents were similar in the normal and stunned myocardium. Water content in the infarcted myocardium (80.8 +/- 2%) was significantly greater (P < .05) than in the normal (72.7 +/- 1.3%), and protein content of 18.5 +/- 0.7% was significantly lower (P < .05) than the normal (21.4 +/- 0.8%). Lipid content was increased in the stunned (8.5 +/- 0.5%) and virtually absent in the infarcted myocardium (0.8 +/- 0.3%) compared with normal (5.5 +/- 0.6%). CONCLUSIONS: We conclude that acoustic propagation properties can identify stunned and infarcted myocardium and may be related to biochemical/morphological differences.

Animals↗
PubMed1999

Electrical impedance properties of normal and chronically infarcted left ventricular myocardium.

BACKGROUND: Previous reports have disclosed that a significant difference exists between the electrical impedance properties of healthy and chronically infarcted ventricular myocardium. PURPOSE: To assess the potential utility of electrical impedance as the basis for mapping in chronically infarcted left ventricular myocardium. Specifically: (1) to delineate electrical impedance properties of healthy and chronically infarcted ventricular myocardium, with special emphasis on the infarction border zone; (2) to correlate impedance properties with tissue histology; (3) to correlate impedance properties with electrogram amplitude and duration; (4) To demonstrate that endocardial impedance can be measured effectively in vivo using an electrode mounted on a catheter inserted percutaneously. METHODS: An ovine model of chronic left ventricular infarction was utilized. Sites of healthy myocardium, densely infarcted myocardium and the infarction border zone were investigated. Bulk impedance was measured in vitro using capacitor cell, four-electrode and unipolar techniques. Epicardial and endocardial impedances were measured in vivo using four-electrode and unipolar techniques. Impedance was measured at multiple frequencies. Electrographic amplitude, duration and amplitude/duration ratio were measured using bipolar electrograms during sinus rhythm. Quantitation of tissue content of myocytes, collagen, elastin and neurovascular elements was performed. RESULTS: Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the border zone transitioning between healthy myocardium and dense infarction. Decreasing impedance correlated with a decrease in tissue myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as the measurement frequency decreased. Healthy myocardium exhibited a marked frequency dependence in its impedance properties; this phenomenon was not observed in densely infarcted myocardium. There was a direct association between impedance and both electrogram amplitude and amplitude/duration ratio. There was an inverse association between impedance and electrogram duration. Endocardial impedance, measured in vivo using a electrode catheter inserted percutaneously, was demonstrated to distinguish between healthy and infarcted myocardium. CONCLUSIONS: The electrical impedance properties of healthy and infarcted left ventricular myocardium differ markedly. The properties of the infarction border zone are intermediate between healthy and infarcted myocardium. Impedance may be a useful assay of cardiac tissue content and adaptable for cardiac mapping in vivo. Condensed Abstract. To delineate the electrical impedance properties of healthy and chronically infarcted left ventricular myocardium emphasizing the infarction border zone, impedance was measured in chronically infarcted ovine hearts. Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the infarction border zone in transition between healthy myocardium and dense infarction. This correlated with a decreasing myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as measurement frequency decreased. There was a direct association between impedance and electrogram characteristics. Endocardial impedance, measured in vivo using an electrode catheter inserted percutaneously, distinguished between healthy and infarcted myocardium

Action Potentials↗
PubMed1991

Coronary pressure-flow, pressure-function, and function-myocardial oxygen consumption relations in postischaemic myocardium.

STUDY OBJECTIVE: The aim was to study coronary pressure-flow, pressure-myocardial wall motion and myocardial wall motion-myocardial oxygen consumption relations in postischaemic myocardium with prolonged myocardial dysfunction (stunned myocardium) in comparison with normal myocardium. DESIGN: Regional myocardial wall thickening was measured with ultrasonic crystals, and postischaemic myocardial dysfunction was achieved by occlusion of a carotid-left anterior descending coronary artery bypass (15 min) and reperfusion (30 min). Coronary perfusion pressure was decreased in 10 mm Hg steps by constricting the bypass before and after producing postischaemic myocardial dysfunction. At each constriction step, coronary flow, regional wall thickening, and regional myocardial oxygen consumption in the area perfused by the left anterior descending artery were measured. EXPERIMENTAL MATERIAL: 12 anaesthetised open chest mongrel dogs, weighing 12-16 kg, were studied. MEASUREMENTS AND MAIN RESULTS: At the basal level, myocardial wall thickening of postischaemic myocardium was depressed compared to normal myocardium, at 18.5(SD 8.9)% v 1.3(7.1)%, p less than 0.01. With coronary stenosis, wall thickening gradually decreased at a coronary pressure below 60 mm Hg in normal myocardium, but remained unchanged until mean coronary pressure was reduced to 50 mm Hg in postischaemic myocardium. Myocardial wall thickening of postischaemic myocardium was always more depressed than normal myocardium. At any level of coronary pressure, coronary flow in postischaemic myocardium was not different from normal myocardium. There was no difference in regional myocardial oxygen consumption between normal and postischaemic myocardium at any level of coronary pressure. However, regional myocardial oxygen consumption in postischaemic myocardium was higher than in normal myocardium performing similar levels of myocardial wall thickening. CONCLUSION: The coronary pressure-function relation but not the pressure-flow relation changed in postischaemic myocardium after a 15 min coronary occlusion. Regional myocardial oxygen consumption was relatively increased in postischaemic myocardium.

Animals↗
PubMed2002

[Different effects of acetylcholine on the action potential and force contraction in guinea pig atrial and ventricular myocardium].

The purpose of this study was to investigate the different effects of ACh on the action potential and force contraction in guinea pig atrial and ventricular myocardium by using standard microelectrodes and force transducer. The results showed that the duration of the action potential (APD) of atrial myocardium was shortened from 208.57+/-36.05 to 101.78+/-14.41 ms (n=6, P<0.01), and the APD of the ventricular myocardium was shortened from 286.73+/-36.11 to 265.16+/-30.06 ms (n=6, P<0.01).The amplitude of the action potential (APA) of the atrial myocardium was decreased from 88.00+/-9.35 to 62.62+/-20.50 mV (n=6, P<0.01), while the APA of the ventricular myocardium did not change significantly.The force contraction of atrial myocardium was inhibited completely (n=6, P<0.01), while the force contraction of ventricular myocardium was inhibited by 37.57+/-2.58% (n=6, P<0.01). The ACh effects correlated with its concentration. The K(D) of the APD shortening effects in the atrial and ventricular myocardium were 0.275 and 0.575 micromol/L. The K(D) of the negative inotropic in the atrial and ventricular myocardium were 0.135 and 0.676 micromol/L, respectively. The corresponding data points were compared using t test between the atrial and ventricular myocardium, and the differences were significant when the ACh concentration was above 10 nmol/L. Furthermore, atropine (10 micromol/L) and CsCl (20 mmol/L) blocked the effects of 10 micromol/L ACh on the APD of ventricular myocardium, while CdCl2 (0.1 mmol/L) had no influence on these effects. In conclusion, ACh could shorten the action potential duration and inhibit the force contraction of atrial and ventricular myocardium in a concentration-dependent manner. There are differences in the effects of ACh on the atrial and ventricular myocardium. The atrial myocardium is more sensitive to ACh than the ventricular myocardium. It is probable that the muscarinic receptor and the potassium channel, but not the calcium channel, are involved in the ACh-induced shortening of the ventricular APD.

Acetylcholine↗
PubMed2006

Detection of ischemic myocardium with a new hypoxic tissue targeting tracer 99Tc(m)-HL91.

The imaging appearances of 99Tc(m)-HL91, a new hypoxic imaging agent, in ischemic myocardium were studied and the value of 99Tc(m)-HL91 in the evaluation of regional ischemic viable myocardium was explored. Acute myocardial ischemia models were made by coronary artery legations in 18 rats and randomly divided into 2 groups: 99Tc(m)-HL91 group and 99Tc(m)-MIBI group. Evan blue infusion during ischemia and TTC staining after operation were used to delineate the area of ischemic and viable myocardium. The isolated heart was sliced in the short axis and then autoradiography was performed. The electron microscopic examination was also done for the myocardial samples. 99Tc(m)-HL91 and 99Tc(m)-MIBI uptake activities (counts/g) were measured in the area of ischemic myocardium (T) and normal myocardium (NT) separately. The uptake ratios of 99Tc(m)-HL91 and that of 99Tc(m)-MIBI in ischemic myocardium were calculated as T/NT. It was found that the normal myocardium was blue and ischemic or infarct myocardium was negative with Evans blue in all experiment rats. Both the normal and ischemic myocardium was in red color with TTC staining. In the 99Tc(m)-HL91 group the ischemic myocardium showed much higher uptake over normal myocardium, that was demonstrated both in the autoradiography and quantitative analysis. The ischemic/normal activity ratios were 1.634 +/- 0.354. It was suggested that 99Tc(m)-HL91 might accumulate in ischemic and viable myocardium, which is helpful in the evaluation of hypoxic but viable myocardium and potentially used as a imaging agent to assess myocardial viability.

Animals↗
PubMed1996

Firm myocardium in cardiopulmonary resuscitation.

Firm myocardium in cardiopulmonary resuscitation (CPR) is a rarely described yet potentially important condition. To investigate the clinical nature and implications of firm myocardium in CPR, we retrospectively analyzed 59 adult patients with nontraumatic out-of-hospital cardiac arrest who underwent open-chest CPR in the emergency department and had heart consistency recorded. Consistency of the myocardium varied considerably between patients. Firm myocardium was noticed in 36 cases, mainly in the left ventricle (firm myocardium group). The remaining 23 hearts were not firm (soft myocardium group). Some hearts had an increase in their consistency during CPR. Patient characteristics were similar in the two groups. The firm myocardium group showed greater base deficit on arterial blood gas analysis, suggesting more severe ischemic injury. Very firm heart had a close association with an extremely low end-tidal CO2 tension. Histopathological examination revealed hypertrophy and fibrosis common to the two groups. Both groups received similar treatment except for a shorter duration of direct cardiac massage in the firm myocardium group, although a reasonably prolonged effort was made in most cases. The firm myocardium group responded poorly to treatment. Very firm myocardium never contracted, whereas less firm myocardium usually showed some, albeit insufficient, activity. Most cases in the soft myocardium group regained a pulse. Our results suggest that firm myocardium: (1) is common in patients who receive CPR in the emergency department, (2) indicates ischemic contracture, (3) is not uniform in firmness, reflecting the degree of ischemia and (4) is a grave prognostic factor in cardiac resuscitation.

Adult↗
PubMedDate not supplied

Assessment of myocardial viability in dysfunctional myocardium by resting myocardial blood flow determined with oxygen 15 water PET.

BACKGROUND: There is controversy about the role of decreased resting blood flow as the pathophysiologic correlate of hibernating myocardium. The aim of this study was an absolute quantification of volumetric myocardial blood flow (MBFvol) in dysfunctional myocardium with different viability conditions as defined by fluorine 18 deoxyglucose (FDG) positron emission tomography (PET) while taking into consideration the functional recovery after revascularization. The impact of MBFvol in the diagnosis of functional recovery was also investigated. METHODS AND RESULTS: Forty-two patients with severe coronary artery disease and dysfunctional myocardium underwent resting oxygen 15 water PET, as well as FDG PET and technetium 99m tetrofosmin single photon emission computed tomography, all attenuation-corrected. Relative FDG and Tc-99m tetrofosmin uptake (normalized to the segment with 100% Tc-99m tetrofosmin uptake), as well as MBFvol (myocardial blood flow multiplied by the water-perfusable tissue fraction to account for the flow to the entire segment volume), were determined in 18 myocardial segments per patient. Viability in dysfunctional segments (estimated by ventriculography) with reduced Tc-99m tetrofosmin uptake of 70% or lower was classified as viable (FDG >70%, mismatch) or nonviable (FDG < or =70%, match). Fifteen patients underwent revascularization and were followed up. Mismatch segments with improved function were classified as hibernating myocardium. Mean MBFvol in viable myocardium was slightly reduced (0.60 +/- 0.02 mL x min(-1) x mL(-1)) compared with that in normokinetic myocardium (0.64 +/- 0.01 mL x min(-1) x mL(-1)) (P = .036) and was significantly higher than in nonviable myocardium (0.36 +/- 0.01 mL x min(-1) x mL(-1)) (P < .001). Receiver operating characteristic analysis confirmed an FDG uptake greater than 70% as the optimal threshold to predict functional recovery (diagnostic accuracy [ACC], 76%). MBFvol in hibernating myocardium (0.62 +/- 0.04 mL x min(-1) x mL(-1)) was not significantly reduced compared with that in normokinetic myocardium (0.66 +/- 0.02 mL x min(-1) x mL(-1)) and was significantly higher than in persistently dysfunctional myocardium (0.51 +/- 0.04 mL x min(-1) x mL(-1)) (P < .05). The ACC of MBFvol greater than 0.40 mL x min(-1) x mL(-1) as the threshold to predict functional recovery was 61% but did not improve the accuracy of FDG PET by itself. CONCLUSIONS: In patients with severe coronary artery disease and dysfunctional myocardium, MBFvol as determined with O-15 water differs significantly between viable and nonviable myocardium as determined by FDG PET and is not significantly reduced in hibernating compared with normokinetic myocardium. Therefore chronically reduced resting blood flow appears unlikely to be the pathophysiologic correlate of the functional state of hibernation. However, MBFvol does not improve the ACC of FDG PET by itself.

Adult↗
PubMed1991

The stunned and hibernating myocardium: a brief review.

DEFINITIONS: Stunned myocardium is viable myocardium salvaged by coronary reperfusion that exhibits prolonged postischemic dysfunction after reperfusion. Hibernating myocardium is ischemic myocardium supplied by a narrowed coronary artery in which ischemic cells remain viable but contraction is chronically depressed. CLINICAL EVIDENCE: Stunned myocardium has been identified in the following patient groups: (1) thrombolysis or percutaneous transluminal coronary angiography (PTCA) in patients with acute evolving infarction; (2) unstable angina; (3) exercise-induced angina; (4) coronary artery spasm; (5) platelet aggregation or transient thrombosis of a coronary artery; (6) PTCA for chronic myocardial ischemia; and (7) immediately following coronary artery bypass graft (CABG). Evidence of hibernating myocardium (LV dysfunction) is found in the patient with severe coronary artery stenosis, even in asymptomatic patients at rest. Stunned myocardium returns to normal after a prolonged period of time (hours to weeks). Hibernating myocardium returns to normal function rather quickly if the cause is removed. DIFFERENTIATION: Stunned myocardium can be differentiated from hibernating myocardium by three clinical parameters, namely, LV wall motion, myocardial perfusion, and myocardial metabolism. Stunned myocardium has abnormal wall motion that tends to normalize in response to inotropes and postextrasystolic potentiation. Perfusion is adequate and metabolism is also adequate. Hibernating myocardium also has abnormal wall motion, which normalizes after nitrates, inotropes, post extrasystolic potentiation (PESP), PTCA, or CABG. Myocardial perfusion is reduced but can be reversed with PTCA or CABG and metabolism is adequate.

Animals↗
PubMed2000

T1-relaxation kinetics of extracellular, intracellular and intravascular MR contrast agents in normal and acutely reperfused infarcted myocardium using echo-planar MR imaging.

The objective of this study was to determine and compare if MR contrast agents distributed into various compartments can provide estimation of fractional distribution volume (FDV) in normal and infarcted myocardium using inversion recovery echo-planar MR imaging (IR EPI). Three different types of MR agents were investigated: (a) an extracellular agent, GdDTPA-BMA (0.1 mmol/kg); (b) an intravascular agent, GdDTPA-albumin (0.025 mmol/kg); and (c) an intracellular agent, manganese chloride (0.025 mmol/kg). The null point was determined from a series of IR EPI images in which TI was varied. Temporal changes in DeltaR1 (DeltaR1 = 1/T1(post)-1/T1(pre)) were measured during the initial 29-59 min after administration. Rats (n = 24) were subjected to 1-h coronary artery occlusion/reperfusion. Histochemical staining confirmed the presence and location of infarction. GdDTPA-BMA caused increase in DeltaR1 of infarction < blood < < normal myocardium. DeltaR1 ratios were 1.55 +/- 0.08 for infarction and 0.33 +/- 0.03 for normal myocardium, consistent with FDV of 0.82 +/- 0.04 and 0.18 +/- 0.01. The fractional distribution of this agent in normal myocardium approximated the extracellular space of myocardium. GdDTPA-albumin caused increase in DeltaR1 of blood < < infarction < < normal myocardium. DeltaR1 ratio in normal, but not infarcted, myocardium was constant at 0.10 +/- 0.02 and approximated fractional blood volume. MnCl(2) caused equivalent increase in DeltaR1 of normal and infarcted myocardium. DeltaR1 of normal myocardium did not change overtime, whereas DeltaR1 of blood rapidly decreased, leading to overestimation of FDV in normal and infarcted myocardium. In conclusion, extracellular, intravascular and intracellular MR contrast agents exhibited different T1-relaxation kinetics in both normal and infarcted myocardium. Constant DeltaR1 ratio (myocardium/blood) after administration of MR contrast agent is a prerequisite for estimation of FDV of MR contrast agent in myocardium.

Albumins↗
PubMed2001

Conotruncal myocardium arises from a secondary heart field.

The primary heart tube is an endocardial tube, ensheathed by myocardial cells, that develops from bilateral primary heart fields located in the lateral plate mesoderm. Earlier mapping studies of the heart fields performed in whole embryo cultures indicate that all of the myocardium of the developed heart originates from the primary heart fields. In contrast, marking experiments in ovo suggest that the atrioventricular canal, atria and conotruncus are added secondarily to the straight heart tube during looping. The results we present resolve this issue by showing that the heart tube elongates during looping, concomitant with accretion of new myocardium. The atria are added progressively from the caudal primary heart fields bilaterally, while the myocardium of the conotruncus is elongated from a midline secondary heart field of splanchnic mesoderm beneath the floor of the foregut. Cells in the secondary heart field express Nkx2.5 and Gata-4, as do the cells of the primary heart fields. Induction of myocardium appears to be unnecessary at the inflow pole, while it occurs at the outflow pole of the heart. Accretion of myocardium at the junction of the inflow myocardium with dorsal mesocardium is completed at stage 12 and later (stage 18) from the secondary heart field just caudal to the outflow tract. Induction of myocardium appears to move in a caudal direction as the outflow tract translocates caudally relative to the pharyngeal arches. As the cells in the secondary heart field begin to move into the outflow or inflow myocardium, they express HNK-1 initially and then MF-20, a marker for myosin heavy chain. FGF-8 and BMP-2 are present in the ventral pharynx and secondary heart field/outflow myocardium, respectively, and appear to effect induction of the cells in a manner that mimics induction of the primary myocardium from the primary heart fields. Neither FGF-8 nor BMP-2 is present as inflow myocardium is added from the primary heart fields. The addition of a secondary myocardium to the primary heart tube provides a new framework for understanding several null mutations in mice that cause defective heart development.

Animals↗
PubMed2002

[Viable myocardium: comparative evaluation of surgical and pharmacological treatment of patients with ischemic heart disease, post-infarct cardiosclerosis and chronic cardiac failure].

AIM: To compare surgical and drug therapies of viable myocardium in IHD patients with left ventricular dysfunction (LVD), to show how to choose between them basing on the presence or absence of viable myocardium in the dyssenergy zones in such patients. MATERIAL AND METHODS: The study enrolled 55 IHD patients with postinfarction cardiosclerosis, left ventricular ejection fraction under 35%, circulatory disorder class I-III (NYHA classification). Coronary artery bypass operation (CABO) was made in 24 patients, 31 patients received drugs. The examination included dobutamin echo-CG, perfusion myocardial scintigraphy. Viability of the myocardium was assessed before and 6 months after the treatment. RESULTS: The patients were divided by the treatment and number of segments of viable myocardium: group 1--patients with viable myocardium subjected to CABO, group 2--patients with non-viable myocardium subjected to CABO, group 3--patients with viable myocardium treated with drugs, group 4--patients with non-viable myocardium treated with drugs. The greatest rise in LV EF, reduction of the end diastolic volume, end systolic volume of the left ventricle and functional class was observed in group 1. In group 2 these parameters changed less than in group 3. Patients of groups 2 and 4 were similar by parameters of LV global contractility. CONCLUSION: Improvement of central hemodynamics and functional class was the greatest in IHD patients after CABO having viable myocardium. If myocardium is not viable surgical treatment has no advantage over conservative in improvement of the pump cardiac function and is inferior to pharmacological treatment in effect on myocardium function in patients with viable myocardium in dyssynergia zones.

Adrenergic beta-Antagonists↗
PubMed1995

[8%-9% and 12%-13% hypoxic gas induced free radicals generation in rat's left and right myocardium].

Alpha-phenyl-tert-butylnitrone (PBN) was administered intravenously to capture free radicals of rat's myocardium. Rats were exposed to hypoxic gas (8%-9% O2 in N2) for 15 min. The ESR (electron spin resonance) signal intensity of PBN-spin adduct in the left myocardium increased significantly as compared with the normoxia group (n = 5, P < 0.05), but in the right myocardium there was no significant changes between hypoxia and normoxia. Rats exposed to hypoxic gas (12%-13% O2 in N2) were divided into four groups: I (hypoxia for 15 min), II (hypoxia for 60 min), III (hypoxia for 30 min/normoxia for 15 min/hypoxia for 30 min) and IV (injected MPEG- SOD intravenously before hypoxia for 60 min). The ESR signal intensity of PBN-spin adduct of left and right myocardium in group II increased significantly as compared with normoxia group (n = 5, P < 0.01), but the ESR signal intensity of group I didn't show obvious change as compared with normoxia group (n = 5, P > 0.05). In the right myocardium of group III the ESR signal intensity of PBN-spin adduct decreased significantly as compared with group II (n = 5, P < 0.05) and in the left myocardium did not decrease evidently. In the left myocardium of group IV the ESR signal intensity of PBN-spin adduct decreased evidently as compared with group II (n = 5, P < 0.05) and that in the right myocardium did not decrease evidently. When the rats were exposed to 8%-9% hypoxic gas for 15 min and 12%-13% hypoxic gas for 60 min, the SOD (superoxide dismutase, EC 1.11.1.9) activity of myocardium decreased and the content of MDA (malondialdehyde) increased significantly (n = 8, P < 0.05 or P < 0.01). The above results suggested that one way of myocardium free radical gereration may be relevant to decrease of SOD activity. The generation of free radicals pertained chiefly to superoxide free radical in the left myocardium and the membrane structure of myocardium cells might have been damaged largely during hypoxia.

Animals↗
PubMed1998

Physiological and biochemical adrenergic regulation of the stunned myocardium.

A dual approach was employed to study beta-adrenergic receptor signal transduction in post ischemic (stunned) myocardium, examining physiological interventions in awake, chronically instrumented pigs and biochemical, cellular mechanisms in sarcolemmal preparations from the stunned hearts using the contralateral non-ischemic zone as a control. Ten min of coronary artery occlusion (CAO) and 30 min coronary artery reperfusion (CAR) resulted in depressed posterior wall-thickening (myocardial stunning). Isoproterenol increased transmural wall thickening more in stunned myocardium than in non-ischemic myocardium. In contrast, the responses of wall thickening to forskolin, actually decreased during stunning compared with control. NKH 477, a water soluble forskolin derivative, that does not activate cardiac nerves, increased wall thickening in non-ischemic tissue similarly to the effects on stunned myocardium. Increasing cardiac neural tone reflexly with inferior venal caval occlusion (IVCO) elicited similar results to forskolin, i.e., stunned myocardium responded with less of an increase in wall thickening as compared with non-ischemic myocardium. Beta-adrenergic receptor density, as determined with 125I-cyanopindolol binding, was significantly increased in stunned subendocardium and subepicardium compared with respective values in non-ischemic myocardium. There were no differences in the response of adenylyl cyclase to isoproterenol in stunned and non-ischemic myocardium. The enhanced responsiveness of the beta-adrenergic receptor to isoproterenol stimulation in stunned myocardium corresponded to the increase in beta-adrenergic receptor density. The combination of enhanced responses to isoproterenol, and decreased responses to forskolin and to IVCO and preserved responsiveness to NKH 477, suggest that stunned myocardium is characterized by transient sympathetic neural stunning. The enhanced sensitivity to beta-adrenergic receptor stimulation has important clinical implications, both in terms of therapy of stunned myocardium and detection of stunned and/or hibernating myocardium, i.e., low dose dobutamine echocardiography.

Adenylyl Cyclases↗
PubMed1999

Ca(2+) sensitization and diastolic function of normal and stunned porcine myocardium.

Ca(2+) sensitizers prolong myofibrillar force development in vitro and might therefore aggravate relaxation abnormalities of stunned myocardium. This is the first in vivo study of the effects of the thiadiazinone derivative EMD 60263 ((+)-5-(l-(alpha-ethylimino-3, 4-dimethoxybenzyl)-1,2,3,4-tetrahydroquinoline-6-yl)-6-methyl-3, 6-dihydro-2H-1,3,4-thiadiazine-2-on), a Ca(2+)-sensitizing agent with negligible phosphodiesterase III inhibitory activity, on diastolic function of regionally stunned myocardium. After producing stunning by two sequences of 10-min coronary artery occlusion and 30 min of reperfusion, anaesthetised pigs received either saline (n=7) or 1.5 and 3.0 mg/kg of EMD 60263 (n=8) or its enantiomer EMD 60264 (n=6), which lacks the Ca(2+)-sensitizing properties but shares the bradycardiac action via inhibition of the delayed inward rectifier K(+) current. In stunned myocardium, systolic shortening was reduced to 46+/-4% of baseline (P<0.05) and mean rate of half end-diastolic segment lengthening, an index for diastolic function, to 35+/-4%; systolic shortening and mean rate of half end-diastolic lengthening of remote normal myocardium remained unchanged. Saline did not affect these parameters in stunned or normal myocardium. EMD 60264 did not affect systolic shortening but decreased mean rate of half end-diastolic lengthening in normal myocardium to 61+/-8% and in stunned myocardium to 16+/-5% of baseline. During saline and EMD 60264, normal and stunned segments started to lengthen immediately after minimal segment length was reached (DeltaT=0). Low dose EMD 60263 restored systolic shortening of the stunned region with no effect on DeltaT. The high dose increased systolic shortening above baseline and DeltaT to 210+/-30 ms in both regions. Consequently, mean rate of half end-diastolic lengthening increased to 66+/-11% in stunned, while decreasing to 55+/-3% in normal myocardium. After elimination of bradycardia, DeltaT and hence mean rate of half end-diastolic lengthening recovered in stunned myocardium, but in normal myocardium the latter remained depressed because DeltaT persisted. In conclusion, both doses of EMD 60263 improved systolic as well as diastolic function of stunned myocardium. The high dose delayed relaxation of normal myocardium without adversely affecting systolic function.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

Extension of borderzone myocardium in postinfarction dilated cardiomyopathy.

This study tests the hypothesis that hypocontractile, borderzone myocardium adjacent to an expanding infarct becomes progressively larger and more hypocontractile as remodeling continues. Early infarct expansion following anteroapical myocardial infarction (MI) is associated with progressive ventricular dilation and heart failure. The contribution of perfused, hypocontractile, borderzone myocardium to this process is unknown. Using a sheep model of anteroapical infarction, sonomicrometry array localization and serial microsphere injections were used to track changes in regional myocardial contractility, geometry, and perfusion. Eight sheep were studied before and after infarction and two, five, and eight weeks later. Thirty intertransducer chord lengths were analyzed to measure regional contractility and serial changes in regional geometry at end systole. Beginning as a narrow band of fully perfused hypocontractile myocardium adjacent to the infarction, borderzone myocardium extends to involve additional contiguous myocardium that progressively loses contractile function as the heart remodels. Three distinct myocardial zones develop as a result of transmural MI: infarct, borderzone (perfused but hypocontractile), and remote (perfused and normally functioning).This study demonstrates that hypocontractile, fully perfused borderzone myocardium extends to involve contiguous normal myocardium during postinfarction remodeling. This borderzone myocardium is a unique type of perfused, hypocontractile myocardium, which is distinct from hibernating or stunned myocardium. Preventing extension of borderzone myocardium by medical or surgical means offers the prospect of preventing late-onset heart failure following transmural expanding MIs.

Animals↗
PubMed2000

Ca(2+) handling in isolated human atrial myocardium.

Physiologically, human atrial and ventricular myocardium are coupled by an identical beating rate and rhythm. However, contractile behavior in atrial myocardium may be different from that in ventricular myocardium, and little is known about intracellular Ca(2+) handling in human atrium under physiological conditions. We used rapid cooling contractures (RCCs) to assess sarcoplasmic reticulum (SR) Ca(2+) content and the photoprotein aequorin to assess intracellular Ca(2+) transients in atrial and ventricular muscle strips isolated from nonfailing human hearts. In atrial myocardium (n = 19), isometric twitch force frequency dependently (0. 25-3 Hz) increased by 78 +/- 25% (at 3 Hz; P < 0.05). In parallel, aequorin light signals increased by 111 +/- 57% (P < 0.05) and RCC amplitudes by 49 +/- 13% (P < 0.05). Similar results were obtained in ventricular myocardium (n = 13). SR Ca(2+) uptake (relative to Na(+)/Ca(2+) exchange) frequency dependently increased in atrial and ventricular myocardium (P < 0.05). With increasing rest intervals (1-240 s), atrial myocardium (n = 7) exhibited a parallel decrease in postrest twitch force (at 240 s by 68 +/- 5%, P < 0.05) and RCCs (by 49 +/- 10%, P < 0.05). In contrast, postrest twitch force and RCCs significantly increased in ventricular myocardium (n = 6). We conclude that in human atrial and ventricular myocardium the positive force-frequency relation results from increased SR Ca(2+) turnover. In contrast, rest intervals in atrial myocardium are associated with depressed contractility and intracellular Ca(2+) handling, which may be due to rest-dependent SR Ca(2+) loss (Ca(2+) leak) and subsequent Ca(2+) extrusion via Na(+)/Ca(2+) exchange. Therefore, the influence of rate and rhythm on mechanical performance is not uniform in atrial and ventricular myocardium.

Aequorin↗
PubMed1995

Tension-frequency relationships in normal and cardiomyopathic dog and hamster myocardium.

The objective of this study was to evaluate the tension-frequency relationship in normal and cardiomyopathic myocardium from one species with a negative or biphasic relationship, the hamster, and one with a positive relationship, the dog. Left ventricular papillary muscles from 100-day-old normal Syrian and cardiomyopathic (CHF-147) hamsters and right ventricular papillary muscles or trabeculae from normal mongrel dogs and dog with pacing-induced heart failure were used for the study. Stimulation frequency was varied from 1 to 90/min and isometric contractions recorded at each frequency prior to and after the addition of phenylephrine 10 microM. A tension-frequency relationship at varying extracellular calcium concentrations (1.25, 2.5 and 5.0 mM) was also constructed in normal hamster myocardium. Ryanodine 1.2 microM was added to a bath with normal hamster muscles and a force-frequency relationship constructed prior to and after adding phenylephrine 10 microM. A calcium dose-response curve in normal and cardiomyopathic dog myocardium was also constructed. Normal and cardiomyopathic hamster myocardium had a biphasic tension-frequency relationship with the increase in tension during the second phase being greater in normal v cardiomyopathic hamster myocardium (0.66 +/- 0.19 v 0.12 +/- 0.03 g/mm2, P < 0.05). The initial decrease in tension in response to increasing stimulation frequency was markedly attenuated in normal hamster myocardium by increasing extracellular calcium concentration. Developed tension was eliminated at lower stimulation rates by ryanodine such that when developed tension did occur, it increased with increasing stimulation rates. The addition of phenylephrine to hamster myocardium modified the tension-frequency relationship of both normal and cardiomyopathic dog myocardium and their response to phenylephrine were similar. In each case, tension increased progressively with increasing stimulation rate. Although the absolute increase in tension caused by increasing extracellular calcium was less in cardiomyopathic dog myocardium, the percent increase in tension and shortening was greater. We conclude that the tension-frequency relationship of normal and cardiomyopathic hamster myocardium are biphasic, with the initial negative phase being the result of limitations of sarcoplasmic reticulum calcium handling. Phenylephrine modifies this relationship to a uniphasic positive one, likely by its effects on both the sarcolemma and the sarcoplasmic reticulum. Also, the tension-frequency relationship of normal and cardiomyopathic dog myocardium are similar and unmodified by phenylephrine.

Animals↗
PubMed2006

[Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine].

OBJECTIVE: To evaluate the effect of adenosine on endothelin-1 (ET-1) after acute myocardial infarction (AMI) and reperfusion and explore the possible mechanism of no-reflow. METHODS: Twenty-four mini-swine were randomized into three study groups: control group (n=8), adenosine treated group (n=8), and sham-operated group (n=8). The mini-swine in the groups were subjected to 3 hours of coronary occlusion, followed by 60 minutes of reperfusion except those in the sham-operated group. The levels of ET-1 in blood sample, normal, infracted reflow and no-reflow myocardium were evaluated by radioimmuno-assay (RIA). The gene expressions of ET-1 in normal, infracted reflow and no-reflow myocardium were quantified by reverse transcription-polymerase chain reaction. RESULTS: In both control group and adenosine group, compared with that at the baseline, ET-1 in blood sample significantly increased at 5 minutes and 180 minutes of left anterior descending coronary artery occlusion, as well as 5 and 60 minutes of reperfusion (all P < 0.01). In adenosine group, the levels of ET-1 were significantly lower than those in the control group (P < 0.05, P < 0.01). In both control group and adenosine group, compared with that in normal myocardium, ET-1 levels in both infarcted reflow and no-reflow myocardium significantly increased (both P < 0.01), with the level of ET-1 in no-reflow myocardium significantly higher than that in infarcted reflow myocardium (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). In both control and adenosine groups, compared with that in normal myocardium, the gene expression of ET-1 in infarcted reflow myocardium was significantly up-regulated (P < 0.01), while that of ET-1 in. no-reflow myocardium significantly down-regulated (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). CONCLUSION: The endothelium injury may be one of the important mechanisms for no-reflow phenomenon. Adenosine cay prevent endothelium from injury to reduce no-reflow.

Adenosine↗