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PubMed2005

Action potential duration and QT interval during pinacidil infusion in isolated rabbit hearts.

INTRODUCTION: Acute myocardial ischemia, which opens K(ATP) channel, is associated with shortened action potential duration (APD) but prolonged QT interval. This discrepancy has not been adequately explained. We hypothesize that the duration of intracellular calcium (Ca(i)) transient (DCaT) may play a role in determining QT interval. METHODS AND RESULTS: We performed simultaneous optical mapping of voltage and Ca(i) in 15 isolated rabbit hearts during a K(ATP) channel opener (pinacidil) infusion. Anterior epicardial mapping (n = 7) showed no difference of APD(90), QT interval, and the DCaT(90) at baseline. When perfused with 80 microM pinacidil, the APD(90), the QT interval, and the DCaT(90) were 105 +/- 10 msec, 199 +/- 14 msec, and 189 +/- 13 msec, respectively, during right ventricular (RV) pacing (P < 0.05). Posterior epicardial mapping (n = 4) showed that the APD(90) was significantly (P < 0.05) shorter than QT interval and DCaT(90) during pinacidil infusion. The results of the transmural mapping studies (n = 4) showed that the QT interval during RV pacing was not different than the DCaT(90) in the epicardium, midmyocardium, and endocardium, but was significantly (P < 0.01) longer than the APD(90) in epicardium, midmyocardium, and endocardium, respectively. There was a good correlation between the DCaT(90) and QT interval at baseline (r = 0.92, P < 0.0001) and during pinacidil infusion (r = 0.74, P < 0.0001). CONCLUSION: We conclude that K(ATP) channel opening shortened APD but not the QT interval. Because Ca(i) did not return to diastolic level at the end of action potential, it may have created a heterogeneous membrane potential distribution that determined the QT interval.

Action Potentials↗
PubMed1988

Localization of 125I-labelled alpha-r-atrial natriuretic peptide in rat tissues by whole-body and microautoradiography.

125I-labelled alpha rat atrial natriuretic peptide (28 amino acids: Ser 99-Tyr 126) ([125I]alpha-rANP) was given i.v. to Sprague-Dawley rats and the distribution of radioactivity in the tissues was examined by whole-body and microautoradiography at intervals from 2 min to 4 h after the administration. Inhibition of uptake of the [125I]alpha-rANP by simultaneous injection of an excess of non-labelled alpha-rANP was taken as an indication that highly labelled structures in rats injected with [125I]alpha-rANP alone are due to an abundance of specific receptors for the peptide. In the rats given only the [125I]alpha-rANP a rapid and high radioactivity occurred in the renal glomeruli, the endocardium of the heart ventricles, the endothelium of the processus ciliares of the eyes, the portal vessels and a few larger vessels of the liver, the subcapsular vessels of the adrenal glands and the parenchyma of the lungs. Other tissues showing a distinct, but less prominent, radioactivity were the endocardium of the heart atria, the walls of the great afferent and efferent vessels in the thoracic cavity, the choroid plexuses of the brain ventricles, the pia mater, brown fat, the muscularis layer of the stomach and the intestines, the lamina propria of the villi in the small intestine and the walls of a few small blood vessels in the kidney medulla. The specific labelling was highest at 2 min after injection and then diminished at later intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Thyroid status and diabetes modulate regional differences in potassium currents in rat ventricle.

1. The rate dependence and recovery kinetics of the Ca(2+)-independent transient (I(t)) and steady-state or 'pedestal' (Iss) outward potassium (K+) currents were studied in single myocytes isolated from epicardial and endocardial regions of rat left ventricles. The whole-cell, suction microelectrode method was used to measure baseline (fully reactivated) I(t), as well as its rate-dependent attenuation. Results from a group of control animals were compared with data from three other groups having an experimentally altered hormonal status. 2. I(t) was significantly smaller in endocardial cells than in epicardial cells, in part due to a very large difference in the recovery kinetics of this current in endocardial cells. This was reflected in a pronounced rate-dependent prolongation of endocardial action potentials. In contrast, the non-inactivating 'pedestal' current, Iss, was very similar in magnitude and showed comparable rate dependence in cells from both epicardium and endocardium. 3. Changing the thyroid status had selective, differential actions on the amplitude and rate dependence of It in epicardial and endocardial cells. Under hypothyroid conditions there was a more pronounced reduction of baseline I(t) in epicardial than in endocardial cells. Moreover, a slowing of the recovery kinetics in epicardial cells resulted in an enhanced attenuation of this current at high rates. Changing thyroid status had no effect on the magnitude or rate dependence of Iss in cells from either region of the left ventricle. 4. Following establishment of hyperthyroid conditions, there was no significant change in I(t) magnitude at baseline. However, when compared with control data, the recovery of I(t) was considerably faster in endocardial cells, and marginally faster in epicardial cells. 5. Streptozotocin-induced diabetic conditions resulted in a much greater attenuation of I(t) in epicardial cells than in endocardial cells. Epicardial action potentials in these conditions showed prominent rate-dependent prolongation. Iss was reduced to a similar extent in cells from these two regions. 6. Our findings demonstrate that altered hormonal status can selectively change the amplitude and kinetics of It in the epi- and endocardium of rat left ventricle. These changes can reduce the epicardial-endocardial gradients in the magnitude and recovery kinetics of It and hence diminish the intrinsic differences in both action potential duration and refractoriness.

Action Potentials↗
PubMed1999

The effects of cross-fiber deformation on axial fiber stress in myocardium.

We incorporated a three-dimensional generalization of the Huxley cross-bridge theory in a finite element model of ventricular mechanics to examine the effect of nonaxial deformations on active stress in myocardium. According to this new theory, which assumes that macroscopic tissue deformations are transmitted to the myofilament lattice, lateral myofilament spacing affects the axial fiber stress. We calculated stresses and deformations at end-systole under the assumption of strictly isometric conditions. Our results suggest that at the end of ejection, nonaxial deformations may significantly reduce active axial fiber stress in the inner half of the wall of the normal left ventricle (18-35 percent at endocardium, depending on location with respect to apex and base). Moreover, this effect is greater in the case of a compliant ischemic region produced by occlusion of the left anterior descending or circumflex coronary artery (26-54 percent at endocardium). On the other hand, stiffening of the remote and ischemic regions (in the case of a two-week-old infarct) lessens the effect of nonaxial deformation on active stress at all locations (9-32 percent endocardial reductions). These calculated effects are sufficiently large to suggest that the influence of nonaxial deformation on active fiber stress may be important, and should be considered in future studies of cardiac mechanics.

Coronary Vessels↗
PubMed1986

Chronic anthracycline cardiotoxicity: haemodynamic and histopathological manifestations suggesting a restrictive endomyocardial disease.

Of 38 patients referred with suspected cardiotoxicity after administration of antineoplastic drugs, 11 patients with signs of manifest or latent anthracycline cardiotoxicity were selected for heart catheterisation with endomyocardial biopsy. Ultrastructural abnormalities of the myocytes with myofibrillar loss and cytoplasmic vacuolation were present in most patients and these findings were more pronounced in biopsy specimens from the left ventricle. Surprisingly, light microscopy showed considerable fibrous thickening of the endocardium in 10 of 11 patients, primarily in the left ventricle. These morphological findings together with the echocardiographic and the haemodynamic data suggest that chronic anthracycline cardiotoxicity is a restrictive endomyocardial disease. The biochemical mechanisms responsible for endocardial fibrosis are unknown, but drug induced damage to the endocardium, possibly mediated via hormonal or humoral agents, may feature in the initial phase of the toxic process. The present observations contribute toward the understanding of the pathophysiology of human anthracycline cardiotoxicity.

Adult↗
PubMed1995

Age-related changes in electrophysiological responses to muscarinic receptor stimulation in rat myocardium.

Recent studies have demonstrated that the negative chronotropic and inotropic responses of the heart to cholinergic muscarinic receptor stimulation are strikingly enhanced with aging in the rat model. The present study investigated the electrophysiological basis of this phenomenon by determining the effects of a muscarinic receptor agonist, carbachol, on transmembrane action potential parameters in right atrial tissue and right ventricular free wall preparations from adult (6-8 months old) and aged (26-28 months old) Fischer 344 rats. In addition, the effect of carbachol on atrioventricular conduction time (AVT) was determined in isolated perfused beating hearts. The results showed the following. The baseline maximum diastolic potential (MDP: adult, -76.4 +/- 1.8 mV; aged, -66.8 +/- 1.5 mV; p < 0.05; n = 5) but not the action potential duration measured at 95% repolarization (APD95: adult, 40.0 +/- 5.0 ms; aged, 47.4 +/- 6.7 ms; n = 5) differed significantly in aged compared with adult atrium. No significant age-related difference was evident in baseline MDP measured in ventricular epicardium (adult, -69.8 +/- 0.5 mV; aged, -69.0 +/- 1.1 mV; n = 6) or endocardium (adult, -72.5 +/- 1.4 mV; aged, -73.0 +/- 1.2 mV; n =6). The baseline action potential duration measured at 50% repolarization (APD50) differed significantly with age in ventricular endocardium (adult, 11.6 +/- 2.2 ms; aged, 23.0 +/- 4.6 ms; p < 0.05; n =6) but not in epicardium (APD50: adult, 8.1 +/- 0.4 ms; aged, 13.0 +/- 2.3 ms; n = 6). Superfusion with carbachol (0.1 nM - 10 mu M) resulted in concentration-dependent hyperpolarization of MDP in atrium; the magnitude of hyperpolarization differed significantly with age (2.5-fold higher in the aged; p < 0.05; n = 5). Carbachol caused concentration-dependent shortening of APD50; this effect differed significantly with age in the ventricle (2-fold greater in the aged; p < 0.05; n = 6) but not in the atrium. Carbachol prolonged the AVT in atrial-paced (240 beats/min) hearts; the magnitude of carbachol-induced increase in AVT did not differ significantly with age. These results are consistent with the possibility that in the aging heart, greater hyperpolarization at the level of the right atrium (likely involving pacemaker cells) and greater shortening of APD50 at the level of ventricular myocytes may contribute to the enhanced cholinergic-triggered bradycardia and negative inotropic response, respectively.

Action Potentials↗
PubMed2002

Purkinje involvement in arrhythmias after coronary artery reperfusion.

Previous studies have indicated that the endocardium may be responsible for a large portion of ventricular tachycardia (VT) seen with reperfusion of ischemic myocardium. To evaluate the role of the Purkinje system in nonreentrant VT arising from the endocardium after reperfusion, the anterior descending coronary artery was occluded for 20 min and then reperfused in 23 dogs after instrumentation of the risk zone with 21 multipolar plunge needles. VT with focal Purkinje origin was defined as a focal endocardial VT with Purkinje potentials recorded before the earliest endocardial myopotential. A total of 19 VTs (mean cycle length 214 +/- 2 ms) were observed with 11 (58%) having focal Purkinje origin. Fifty-eight percent of the VTs degenerated to ventricular fibrillation, with occurrences of two or more independent foci per complex (seen in 7 of 11 compared with 1 of 8 nonsustained VTs). In conclusion, these data show that Purkinje tissue may be important in the genesis of reperfusion VT.

Animals↗
PubMed1980

Left ventricular free wall and intraventricular pressure-sarcomere length distributions.

Sarcomere lengths were measured after pentobarbital anesthesia at five sites through the wall of the formaldehyde solution-fixed cadmium-arrested closed-chest rat left ventricle. Sections (250 micron) were cut from endocardium to epicardium with a freezing microtome. Selected sections were sonified, mixed with a gelatin-water solution, and placed on a glass slide. Sarcomere lengths were measured with an optical microscope at five sites through the wall. Sarcomere lengths progressively increased from section I (endocardium site) to section III (middle site) and IV. Sarcomere lengths were again shorter in section V (epicardium site). There was a progressive increase in sarcomere lengths with increasing intraventricular pressures. Sarcomere lengths did not significantly exceed optimum length.

Animals↗
PubMed1989

Nonuniform transmural recovery of contractile function in stunned myocardium.

With the use of an epicardial Doppler probe, systolic wall thickening was selectively measured in the inner, mid, and outer layers of the left ventricular (LV) wall in 16 conscious dogs undergoing a 15-min left anterior descending artery (LAD) occlusion followed by 7 days of reperfusion (REP). Under control conditions, percent thickening fraction (ThF) was significantly greater (P less than 0.01) in the inner layer [36.0 +/- 2.3% (mean +/- SE)] than in the mid (28.6 +/- 2.1%) or outer (21.3 +/- 2.2%) layers. During LAD occlusion, 11 dogs exhibited transmural dyskinesis (group 1), whereas 5 had transmural hypokinesis (group 2). In group 1, all layers exhibited comparable degrees of paradoxical systolic thinning during LAD occlusion. After REP, however, recovery was delayed in the inner compared with the mid and outer layers. At 2 h, ThF averaged 34.2 +/- 11.9% of base line in the endocardium vs. 61.7 +/- 16.2% in the midmyocardium and 51.0 +/- 12.3% in the epicardium (F = 4.29, P less than 0.002); similar differences were noted at 3 and 4 h. In the mid and outer layers, ThF returned to base-line values by 24 h, whereas in the inner layer it was still significantly depressed (P less than 0.05) at 24 h (77.3 +/- 5.1% of base line) and recovered by 48 h. The inner-to-outer ThF ratio was decreased (P less than 0.01) for 24 h after REP, indicating maldistribution of thickening in the "stunned" myocardium. In group 2, all layers exhibited hypokinesis during LAD occlusion. Again, recovery of function after REP was delayed in the endocardium compared with the other layers. This study demonstrates that after both severe ischemia resulting in dyskinesis and mild ischemia resulting in hypokinesis, REP is associated with slower recovery of function in the inner than in the outer layers. Thus myocardial "stunning" is a nonuniform phenomenon with maximal severity in the subendocardium.

Animals↗
PubMed1990

Three-dimensional mapping of acute ischemic regions using MRI: wall thickening versus motion analysis.

Three-dimensional (3D) endocardial wall motion and thickening were compared as quantitative methods for distinguishing ischemic from non-ischemic myocardium and for their potential to map regional left ventricular (LV) function. Data were obtained by gated magnetic resonance (MR) images in seven open-chest dogs with acute ischemia. The LVs were reconstructed in 3D at end diastole (ED) and end systole (ES) with a helical coordinate system that wraps the endocardium and epicardium. Thickness and percent wall thickening were calculated by a 3D volume element method. Wall motion was calculated by the 3D displacement of the endocardium perpendicular to the wall using both fixed and floating centroids. Monastral blue nonstaining identified the ischemic regions from five anatomical slices of the LV, which corresponded to the in vivo image planes. Thickening and motion were compared at the centers of the ischemic and the remote normal zones, in addition to comparing the functional maps of the entire LV to the postmortem anatomical maps. All methods distinguished between the center of the ischemic zone and the remote normal zone; however, thickening discriminated most strongly between zones. Comparison of the 3D in vivo maps with the 3D postmortem maps showed that the sensitivity, specificity, and overall accuracy of the thickening algorithm exceeded those obtained by the wall motion algorithms with fixed or floating centroids. Thus wall thickening utilizing the 3D volume element approach is superior to 3D wall motion algorithms in distinguishing ischemic from nonischemic zones and in mapping regional function in the entire LV.

Acute Disease↗
PubMed1991

Transmural distribution of three-dimensional strain in the isolated arrested canine left ventricle.

Three-dimensional myocardial strains in seven isolated, potassium-arrested dog hearts were measured by biplane radiography of 3 transmural columns of 4-6 radiopaque beads implanted in the midanterior left ventricular free wall. Transmural distributions of strain during inflation of a left ventricular balloon to 20-30 mmHg were computed with respect to the zero pressure state. Magnitudes of the 3 principal strains increased in proportion to ventricular volume (0.0088, 0.0037, and -0.0059 ml-1). At a left ventricular pressure of 8 +/- 4 mmHg, mean circumferential (E11) and longitudinal strains (E22) were similar, increasing from epicardium (0.058 +/- 0.055 and 0.036 +/- 0.024) to subendocardium (0.139 +/- 0.102 and 0.120 +/- 0.084) as did the transmural (wall thinning) strain E33 (-0.053 +/- 0.071 to -0.128 +/- 0.083). Negative in-plane shear E12 was small (-0.008 to -0.052), consistent with a left-handed torsion of the left ventricular wall. Mean transverse shear strains E13 and E23 were small (-0.029 to 0.007) but showed considerable variability between hearts. Fiber strain had no significant transmural variation (P = 0.57). The principal axis of greatest strain was close to the fiber orientation on the epicardium (-15 degrees) but closer to the cross-fiber direction near the endocardium (-40 degrees). Therefore, the end-diastolic fiber lengths are maximized on the epicardium and minimized on the endocardium.

Animals↗
PubMed1992

Porous medium finite element model of the beating left ventricle.

The axisymmetric model described represents myocardial tissue as a spongy anisotropic viscoelastic material. It includes torsion around the axis of symmetry of the ventricle, transmural variation of fiber angle, and redistribution of intracoronary blood in the myocardial wall. In simulations, end-systolic principal strains were equal to 0.45, -0.01, and -0.24 at two-thirds of the wall thickness from the epicardium and 0.26, 0.00, and -0.19 at one-third of the wall thickness from the epicardium. The direction of maximal shortening varied by less than 30 degrees from epicardium to endocardium, whereas fiber direction varied by greater than 100 degrees from epicardium to endocardium. During a normal cardiac cycle peak, equatorial intramyocardial pressure differed by less than 5% from peak intraventricular pressure. When redistribution of intracoronary blood in the ventricular wall was suppressed, peak equatorial intramyocardial pressure was found to exceed peak intraventricular pressure by greater than 30%. Simulated contraction of an unloaded left ventricle (left ventricular pressure = 0 kPa) produced similar magnitude for systolic intramyocardial pressures as the normal cardiac cycle. Transmural systolic fiber stress distribution was very sensitive to the chosen transmural fiber angle distribution.

Animals↗
PubMed1999

Mechanisms of desensitization to a PDE inhibitor (milrinone) in conscious dogs with heart failure.

The goal of this study was to determine the extent to which the effects of milrinone were desensitized in heart failure (HF) and to determine the mechanisms, i.e., whether these effects could be ascribed to changes in cAMP or phosphodiesterase (PDE) activity in HF. Accordingly, we examined the effects of milrinone in seven conscious dogs before and after HF was induced by rapid ventricular pacing at 240 beats/min. The dogs were chronically instrumented for measurements of left ventricular (LV) pressure and first derivative of LV pressure (dP/dt), arterial pressure, LV internal diameter, and wall thickness. Milrinone (10 micrograms . kg-1. min-1 iv) increased LV dP/dt by 1,854 +/- 157 from 2,701 +/- 105 mmHg/s (P < 0.05) before HF. After HF the increase in LV dP/dt in response to milrinone was attenuated significantly (P < 0.05); it increased by 615 +/- 67 from 1,550 +/- 107 mmHg/s, indicating marked desensitization. In the presence of ganglionic blockade the increases in LV dP/dt (+445 +/- 65 mmHg/s) in response to milrinone were markedly less (P < 0.01), and milrinone increased LV dP/dt even less in HF (+240 +/- 65 mmHg/s). cAMP and PDE activity were measured in endocardial and epicardial layers in normal and failing myocardium. cAMP was decreased significantly (P < 0.05) in LV endocardium (-26%) but not significantly in LV epicardium (-14%). PDE activity was also decreased significantly (P < 0.05) in LV endocardium (-18%) but not in LV epicardium (-4%). Thus significant desensitization to milrinone was observed in conscious dogs with HF. The major effect was autonomically mediated. The biochemical mechanism appears to be due in part to the modest reductions in PDE activity in failing myocardium, which, in turn, may be a compensatory mechanism to maintain cAMP levels in HF. Reductions in cAMP and PDE levels were restricted to the subendocardium, suggesting that the increased wall stress and reduced coronary reserve play a role in mediating these changes.

Animals↗
PubMed1999

Ultrastructural assessment of myocardial necrosis occurring during ischemia and 3-h reperfusion in the dog.

To determine whether myocardial necrosis may occur during postischemic reperfusion, electron microscopy was used to identify morphological features of irreversible injury in myocardial samples taken from anesthetized dogs with 90-min ischemia and 0-, 5-, 90-, or 180-min reperfusion. In samples without detectable collateral blood flow, necrosis was almost complete, whether or not the myocardium was reperfused. In samples with collateral flow, necrosis was more frequent after 180-min reperfusion than in the absence of reperfusion, despite similar collateral flows in the two groups. Excess of necrosis after 180-min reperfusion was evident in endocardium (ischemia only: 4 of 13, 180-min reflow: 14 of 20; P = 0. 03) and midwall (ischemia only: 9 of 25, 180-min reflow: 29 of 45; P = 0.02). Multiple logistic regression with variables of collateral flow and transmural position was used to determine risk of irreversible injury in 111 samples from ischemic myocardium without reperfusion (model predictive accuracy = 75%, P < 0.00001) and to predict risk of necrosis in myocardium reperfused for 180 min. Of 65 samples from endocardium and midwall with detectable collateral flow, the model predicted necrosis in 23 samples but necrosis was observed in 43 samples (P < 0.01). Reperfusion duration was a determinant of frequency of irreversible injury. Multiple logistic regression for 186 samples from myocardium reperfused for 5, 90, or 180 min showed that reperfusion duration was an independent predictor of irreversible injury (P = 0.0003) when collateral flow and transmural location were accounted for. These findings are consistent with the occurrence of necrosis during reperfusion in myocardium exposed to substantial, prolonged ischemia but with sufficient residual perfusion to avoid necrosis during the period of flow impairment.

Animals↗
PubMed2006

Increased expression of vascular endothelial growth factor in cardiac structures of fetus with hydrops as compared to nonhydropic controls.

OBJECTIVE: The hypothesis that severe fetal hydrops is caused by an excess of vascular endothelial growth factor (VEGF), mainly produced in the fetal heart, is tested. METHODS: Immunohistochemical VEGF-stained postmortem biopsies from the right ventricle and right atrium of 8 hydropic fetuses were compared to those of 8 nonhydropic fetuses. The endocardium, myocardium, epicardium, endothelium, and vascular smooth muscle cells were scored on intensity of VEGF-staining. The Mann-Witney test was used to test for significancy (p < 0.05) of the differences in staining. Increased vascularization as a result of VEGF was measured in both groups by standard randomization count. RESULTS: The endocardium, epicardium and endothelium of the coronary vessels showed significantly (p < 0.05) more intense VEGF-staining in the hydrops group than in the control group. The atria showed more intense staining than the ventricles in both groups. The hydropic fetuses showed a significantly increased number of coronary vessels in the myocardium. These vessels contained more blood cells than the coronary vessels in nonhydropic fetuses. CONCLUSION: The fetal heart appears to be a major source of excess VEGF in fetal hydrops.

Fetal Heart↗
PubMed2003

Regional alterations in protein expression in the dyssynchronous failing heart.

BACKGROUND: Left ventricular (LV) mechanical dyssynchrony induces regional heterogeneity of mechanical load and is an independent predictor of mortality and sudden death in heart failure (HF) patients. We tested whether dyssynchrony also induces localized disparities in the expression of proteins involved with mechanical stress, function, and arrhythmia susceptibility. METHODS AND RESULTS: Eleven dogs underwent tachycardia-induced HF pacing, either from the right atrium or high right ventricular free wall. Whereas global LV dysfunction was similar between groups, LV contractile coordination assessed by tagged MRI was markedly dyssynchronous with right ventricular pacing but synchronous with right atrial pacing. In dyssynchronous failing hearts, the lateral LV endocardium displayed a 2-fold increase in phosphorylated erk mitogen-activated protein kinase expression (with no change in phospho-p38 or phospho-jnk), a 30% decline in sarcoplasmic reticulum Ca2+-ATPase, an 80% reduction in phospholamban, and a 60% reduction in the gap junction protein connexin43, relative to neighboring myocardial segments. In contrast, hearts from both right atrial-paced HF dogs and an additional 4 noninstrumented control animals showed minimal regional variability in protein expression. CONCLUSIONS: LV dyssynchrony in failing hearts generates myocardial protein dysregulation concentrated in the late-activated, high-stress lateral endocardium. Such molecular polarization within the LV creates transmural and transchamber expression gradients of calcium handling and gap junction proteins that may worsen chamber function and arrhythmia susceptibility.

Animals↗
PubMed2001

Tissue Doppler imaging differentiates transmural from nontransmural acute myocardial infarction after reperfusion therapy.

BACKGROUND: The evaluation of transmural extent of necrosis after acute myocardial infarction remains a major problem in clinical practice. We sought to determine whether color M-mode tissue Doppler imaging (TDI) could differentiate transmural from nontransmural myocardial infarction. METHODS AND RESULTS: Twenty-one anesthetized open-chest dogs underwent 90 or 120 minutes of left anterior descending coronary artery occlusion followed by 180 minutes of reperfusion. The transmural extension of infarct was measured by triphenyltetrazolium chloride (TTC) staining. Segment shortening in the endocardium and epicardium of the anterior and posterior walls was assessed by sonomicrometry. Regional myocardial blood flow was measured by radioactive microspheres. TDI was obtained from an epicardial short-axis view. We calculated systolic and diastolic velocities within the endocardium and epicardium of myocardial walls and the subsequent myocardial velocity gradient (MVG). TTC staining could identify 2 groups according to the transmural extent of necrosis: 15 dogs had a nontransmural (NT) necrosis (42+/-3% of wall thickness), and 6 dogs developed a transmural (T) infarct (81+/-4% of wall thickness). In both groups, ischemia resulted in a significant and similar reduction in endocardial and epicardial velocities, with a resulting low systolic MVG in the anterior wall (0.10+/-0.07 in NT and 0.10+/-0.08 s(-1) in T). At 60 minutes of reperfusion, systolic MVG failed to change significantly in the transmural group (-0.20+/-0.09 s(-1)). In contrast, it increased significantly after reflow in the NT group compared with ischemic values (-0.99+/-0.20 versus 0.10+/-0.07 s(-1), P:<0.05). CONCLUSIONS: TDI can differentiate transmural from nontransmural myocardial infarction early after reperfusion.

Animals↗
PubMed1982

Effects of digitalis on subendocardial and subepicardial dysfunction during acute ischemia.

The effects of digitalis (ouabain infusion, priming dose of 10 micrograms/kg/min followed by 2.0 micrograms/kg/min) on subepicardial and subendocardial ischemic dysfunction during partial occlusion (59.4% reduction in coronary flow) and total coronary occlusion were evaluated in 14 dogs using pairs of ultrasonic crystals implanted in the epicardial and endocardial layers. After 30 minutes of partial coronary occlusion, systolic shortening in the ischemic zone decreased from 12.4 +/- 2.9% to -0.4 +/- 0.9% (p less than 0.001) in the epicardium and from 18.9 +/- 3.1% to -1.0 +/- 1.1% (p less than 0.001) in the endocardium. Ouabain infusion increased the systolic shortening from -0.4 +/- 0.9% to 10.6 +/- 3.1% (p less than 0.001) in the epicardium and from -1.0 +/- 1.1% to 17.2 +/- 3.4% (p less than 0.001) in the endocardium. The end-diastolic length did not change. In contrast, after 30 minutes of total coronary occlusion, systolic shortening in both epicardial and endocardial layers was replaced by systolic lengthening and remained unaffected by ouabain infusion in both layers. Systolic shortening in the nonischemic epicardial and endocardial layers increased consistently. We conclude that ouabain improves the contractile function of both ischemic epicardial and endocardial layers layers after partial coronary occlusion and does not worsen subendocardial ischemic dysfunction. After total coronary occlusion, however, the contraction of the ischemic zone is unaffected by ouabain.

Animals↗