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PubMed1994

Instrumentation of ramus circumflexus compromises the innervation of coronary artery and myocardium.

A fine non-compressing methacrylate ring was implanted on the ramus circumflexus (RC) in 13 dogs. After the animals survived 7-14 days, the distribution and the rate of the Wallerian degeneration was studied in coronary arteries and myocardium by means of the formaldehyde induced fluorescence (FIF) technique and the transmission electron microscopy. The density of vasomotor innervation in the main arterial trunks was expressed as the number of transsected terminals per 1 mm2 of the transversally sectioned media; the density of adrenergic terminals in the myocardium was determined by the point-counting method. A compact scar encompassing the ring was found. The scar compressed some perivascular nerves. As a consequence, by about 40% of terminals degenerated in the RC. The innervation of the branching of this artery was compromised as well. Moreover, the density of nerve terminals in myocardium decreased around the whole circumference of the ventricles and in the septum, equally by 29%. The value was lower than that found after the instrumentation of ramus interventricularis anterior (50%). The results indicate (i) a compromise of the innervation of coronary artery and myocardium after the instrumentation of RC; (ii) the different decrease in density of nerve terminals in the myocardium suggests that majority of adrenergic nerve supply for ventricle myocardium is running along ramus interventricularis anterior.

Animals↗
PubMed1990

In vivo delineation of myocardial hypoxia during coronary occlusion using fluorine-18 fluoromisonidazole and positron emission tomography: a potential approach for identification of jeopardized myocardium.

Previous studies have demonstrated that the positron-emitting fluorine-18 (18F)-labeled fluoromisonidazole is a specific tracer of myocardial hypoxia. Its fractional extraction is enhanced in ischemic or hypoxic myocardium but returns to baseline levels on reperfusion and recovery of normal function. Thus, this agent might be useful in delineating acutely hypoxic but potentially salvageable myocardium. Accordingly, to delineate the relation between the myocardial extraction of 18F-fluoromisonidazole after intravenous administration and the time of antecedent ischemia in vivo, uptake of tracer was measured with positron emission tomography and direct postmortem tissue analysis in 14 dogs in which tracer was administered within 3 h of coronary occlusion (a time associated with marked potential for salvage on reperfusion); in 4 dogs after 6 h of coronary occlusion (a time associated with minimal salvage of myocardium on reperfusion); and in 8 dogs after greater than 24 h of coronary occlusion (to delineate uptake in tissue that is irreversibly damaged). The residual fraction (that is, the amount of tracer extracted and retained in a region) in ischemic myocardium in the dogs in which 18F-fluoromisonidazole was administered within 3 h after occlusion averaged (+/- standard deviation) 23 +/- 18%, which was higher than the residual fraction in myocardium subjected to ischemia for either 6 or greater than 24 h before tracer administration (12 +/- 7% and 5 +/- 2%, respectively, p less than 0.01 for both). Retention of tracer in remote normal myocardium averaged 2 +/- 1%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Enhanced sensitivity of the failing human myocardium to cardiac glycosides and Na(+)-channel activators.

Cardiac glycosides and Na+ -channel activators increase intracellular Na+ and thereby enhance the transport rate of the sarcolemmal Na+/Ca2+ exchanger. We tested the hypothesis of whether increased expression of the Na+/Ca2+ exchanger in failing human myocardium is accompanied by enhanced sensitivity of the failing human myocardium toward cardiac glycosides and Na+ -channel activators. We studied the positive inotropic effects of the new Na+ -channel activator BDF and the cardiac glycoside ouabain in human failing (New York Heart Association [NYHA] functional class IV, heart transplants for dilated cardiomyopathy, n = 11) and nonfailing (donor hearts, n = 5) myocardium on electrically driven left ventricular papillary muscle strips (1 Hz, 37 degrees C). The effectiveness of ouabain and BDF to increase force of contraction was similar in human nonfailing and failing myocardium. BDF was more potent to increase force of contraction in failing than in nonfailing tissue (p < 0.05). The time until maximal inotropic effect developed after ouabain was significantly shorter in NYHA IV (mean 150 +/- 16 min) than in nonfailing myocardium (mean 240 +/- 20 min). These results suggest that human failing myocardium exerts and enhanced sensitivity to cardiac glycosides and Na+ -channel activators, possibly because of enhanced expression of the Na+/Ca2+ exchanger or because of an altered intracellular Na+ -homeostasis.

Adolescent↗
PubMed2001

Restraining acute infarct expansion decreases collagenase activity in borderzone myocardium.

BACKGROUND: After acute myocardial infarction, regional myocardial wall strains and stresses change and a complex cellular and biochemical response is initiated to remodel the ventricle. This study tests the hypothesis that changes in regional ventricular wall strains affect regional collagen accumulation and collagenase activity. METHODS: Fourteen sheep had acute anteroapical infarction that progressively expands into left ventricular aneurysm within 8 weeks. In 7 sheep, infarct expansion was restrained by prior placement of mesh over the area at risk. Fourteen days after infarction, and after hemodynamic and echocardiographic measurements, animals were euthanized for histology, measurements of hydroxyproline, matrix metalloproteinase-1 (MMP-1 or collagenase) and MMP-2 (gelatinase) activity, as well as collagen type I and III in infarcted, borderzone, and remote myocardium. RESULTS: Restraining infarct expansion does not change collagen content or MMP-1 or MMP-2 activity in the infarct, but significantly increases the ratio of collagen I/III. In borderzone and remote myocardium infarct, restraint significantly increases collagen content and significantly reduces MMP-1 activity. MMP-2 activity is reduced (p = 0.059) in borderzone myocardium only. Between groups, the ratio of type I/III fibrillar collagen does not change in borderzone myocardium. CONCLUSIONS: Fourteen days after acute myocardial infarction, restraining infarct expansion increases collagen accumulation in borderzone and remote myocardium, which may prevent expansion of hypocontractile, fully perfused "remodeling myocardium" adjacent to the infarct. This study demonstrates that changes in regional myocardial wall strain alter the cellular and biochemical processes involved in postinfarction ventricular remodeling.

Animals↗
PubMed1976

Electron microscopical and enzyme histochemical changes in the rat myocardium during prolonged autolysis.

The effect on rat myocardium of autolysis at 19 degrees C, for up to 20 days, was studied by electron microscopy and enzyme histochemistry. The enzymes studied included monoamine oxidase (MAO), sytochrome oxidase (CytO), non-specific esterase ((Ns.E.), phosphorylase (P-ase), succinate dehydrogenase (SDH) and various NAD- and NADP-linked dehydrogenases. The myocardium lost its histochemical P-ase activity within a few hours of autolysis, whereas the activity of all other enzymes remained quite normal for at least about 4 days, except that of MAO and SDH, which were normal for about 8 and 12 days, respectively. The myocardial cells lost activity of various enzymes in a patchy manner during prolonged autolysis and practically all histochemical enzyme activity disappeared within 20 days. The early period of autolysis was accompanied by rapid ultrastructural changes of myocardial cells. During prolonged autolysis the gross architecture of the myocardium was lost gradually by the 12th to 20th days. Mitochondria were the organelles most resistant to the effects of autolysis, and numerous mitochondria with morphologically solid inner and outer membranes were seen among the totally disintegrated myocardium 20 days after death. The loss of P-ase activity coincided with the loss of glycogen. The loss of MAO, SDH and CytO activities was not closely related to the morphological preservation of mitochondria, but, in accordance with other enzymes, was more closely related to the disintegration of the over-all myocardial structure. The present results showed that the architecture of the myocardium, and especially that of the mitochondria, was surprisingly resistant to the effects of autolysis at room temperature. Also several enzymes of the myocardium other than those examined so far maintained quite stable histochemically demonstrable activity during prolonged autolysis. These observations give support to the possibility of making the diagnosis of myocardial infarction at postmortem more accurate than with the present morphological and histochemical routine methods.

Alcohol Oxidoreductases↗
PubMed1984

Identification and localization of creatine kinase B and M in normal, ischemic and necrotic myocardium. An immunohistochemical study.

We utilized immunoperoxidase methods to study the distribution of CK-B and CK-M in normal, ischemic and necrotic myocardium. Human myocardium was obtained from autopsy (n = 10) and surgery (n = 16). Cardiac tissue from 22 dogs with experimental myocardial infarction induced by closed-chest coronary balloon occlusion and four dogs with myocardial ischemia without necrosis induced by a 50% reduction in left main coronary artery blood flow for 3 h were studied. Duration of occlusion was 45 min (n = 2), 3 h (n = 8), 5 to 6 h (n = 7), 15 to 24 h (n = 5). Highly purified anti-CK-B and M were prepared in our laboratory and obtained commercially. In all cases, control experiments were performed. Microscopically normal human and dog myocardium uniformly stained for CK-B and CK-M. Necrotic myocardium from patients with acute infarcts (10 to 24 h old) showed markedly reduced immunostaining. In dogs with 3 to 24 h occlusion immunostaining was significantly reduced for both CK-B and CK-M in regions confirmed to be necrotic by triphenyl tetrazolium chloride (TTC) and H & E staining. Myocardial necrosis was confirmed in the 3-h infarcts by electron microscopy (EM). In the four dogs with a 50% reduction in left main flow for 3 h, ischemia was demonstrated by glycogen loss in periodic acid-Schiff stained-sections; but there was no evidence of necrosis by EM or TTC, and there was no loss of immunostaining evident for CK-B and CK-M. Thus, using immunoperoxidase techniques, CK-B and CK-M were visualized in normal and ischemic myocardium, with decreased staining in necrotic tissue. These findings indicate that cell death is necessary for the demonstration of CK-M and CK-B loss from the myocardium by this technique.

Animals↗
PubMed2002

Comparison of the level of mitochondrial DNA A3243G mutation in esophageal epithelium and myocardium from individuals of very advanced age.

The A3243G mutation, one of the changes of human mitochondrial DNA (mtDNA) that accumulates in cells during aging, is a useful marker for investigating the aging of cells. We measured the mutation level of the mtDNA A3243G mutation using DNAs from two different tissues (esophageal epithelium and myocardium) from advanced elderly individuals. The mean level of the A3243G mutation for the esophageal epithelium was 0.0063+/-0.0019, and that for the myocardium was 0.0098+/-0.0031. The mutation level in the myocardium was significantly higher than that in the esophageal epithelium, indicating that more mtDNA A3243G mutations accumulated in the myocardium than in the esophageal epithelium. Since the myocardium is static with respect to cell turnover, but in the esophageal epithelium renewal is very rapid, it is possible that the mtDNA A3243G mutation in the myocardium accumulates more rapidly than in the esophageal epithelium. This phenomenon may reflect the difference in the longevity of cells in each of these tissues and their different levels of oxidative stress.

Aged↗
PubMed2001

Stability of hibernating myocardium in pigs with a chronic left anterior descending coronary artery stenosis: absence of progressive fibrosis in the setting of stable reductions in flow, function and coronary flow reserve.

OBJECTIVES: This study was performed to determine whether hibernating myocardium is adaptive or is destined to undergo progressive irreversible injury. BACKGROUND: Previous studies have suggested that hibernating myocardium eventually results in progressive dysfunction. Since serial studies cannot be performed in humans, the temporal progression of physiologic and structural adaptations was evaluated in pigs with hibernating myocardium. METHODS: Pigs were instrumented with a left anterior descending coronary artery (LAD) stenosis (1.5 mm) and underwent physiologic studies three to five months later to quantify regional function, perfusion and 18F-2-deoxyglucose (FDG) uptake. Viability was confirmed by histology and contractile reserve. RESULTS: Hibernating myocardium was characterized by severe regional dysfunction (centerline score, -1.9+/-0.1), reduced resting subendocardial flow (LAD: 0.85+/-0.03 vs. normal: 1.02+/-0.03 ml/min/g, p < 0.01), critically reduced subendocardial flow reserve (adenosine flow: 1.04+/-0.09 ml/min/g, p = NS vs. rest; epinephrine flow: 0.88+/-0.07 ml/min/g, p = NS vs. rest) and increased FDG uptake (0.022+/-0.002 vs. 0.014+/-0.001 ml/g/min, p < 0.01). Physiologic parameters were not different among animals studied at three (93+/-1 days, n = 27), four (118+/-2 days, n = 26) or five months (150+/-6 days, n = 9). Pathology revealed a small increase in LAD connective tissue (6.4+/-0.4% vs. 4.0+/-0.2%, p < 0.001), with no change over this time frame. CONCLUSIONS: Thus, physiologic and structural features of hibernating myocardium remain constant for at least two months. The absence of functional deterioration or progressive fibrosis suggests that hibernation is adaptive rather than an unstable physiology destined to progress to irreversible injury. The stability of this model appears ideally suited for interventions targeted to improve flow and function in chronically dysfunctional myocardium.

Animals↗
PubMed1984

Reductions in coronary flow under resting conditions in collateral-dependent myocardium of patients with complete occlusion of the left anterior descending coronary artery.

Flow per unit weight in collateral-dependent myocardium was quantified selectively in seven patients with complete occlusion of the proximal left anterior descending artery and prominent distal collateralization from the right coronary artery by infusing dissolved hydrogen into the right coronary artery for 10 to 15 minutes and monitoring hydrogen desaturation in the great cardiac vein. Coronary flow per unit weight in all myocardium draining into the great cardiac vein was quantified simultaneously by having the patient breathe helium and by monitoring arterial and great cardiac vein helium desaturation. Flow per unit weight in collateral-dependent myocardium averaged 38 +/- 8 (standard deviation) ml/min per 100 g and was in each case below the 95% confidence limit for normal individuals with the same rate-pressure product. Flow per unit weight in all myocardium draining into the great cardiac vein was systematically higher (51 +/- 8 ml/min per 100 g); because arteries other than the anterior descending had no stenoses greater than 30% in diameter, these values presumably reflect mixtures of subnormally perfused collateralized myocardium and adjacent normally perfused tissue. The findings suggest that coronary flow per unit weight is not maintained at usual basal values in densely collaterlized myocardium that is entirely collateral-dependent. The reductions in flow are presumably associated with marked reductions in local arterial pressure and raise the possibility of a chronic reduction in local myocardial metabolic demand.

Adult↗
PubMed1997

Myocardial cell death and apoptosis in hibernating myocardium.

OBJECTIVES: This study was designed to study apoptosis in hypoperfused hibernating myocardium subtending severe coronary stenosis. BACKGROUND: Apoptosis contributes to myocyte death in acute myocardial infarction. METHODS: A left anterior descending coronary artery stenosis was created in 13 pigs and maintained for 24 h (n = 4), 7 days (n = 5) and 4 weeks (n = 4) to reduce coronary blood flow by a mean of 34% with severe regional myocardial systolic dysfunction, as documented by echocardiography. Apoptosis was detected with an in situ end-labeling method and confirmed by "deoxyribonucleic acid laddering" on agarose-gel electrophoresis. The severity of apoptosis was expressed as the percentage of apoptotic myocyte nuclei and nonapoptotic myocardial nuclei. RESULTS: Myocardial blood flow of the anterior left ventricular wall was reduced from 1.00 +/- 0.18 to 0.66 +/- 0.21 ml/min per g (p < 0.01), with a severe reduction of anterior regional wall thickening from a mean (+/-SD) of 39 +/- 4% to 9 +/- 8% (p < 0.01). There was no myocardial infarction in five pigs and minimal patchy infarction of < or = 6% of the area at risk in eight pigs. Apoptotic myocytes were observed in the hibernating myocardial region in all pigs (4.8 +/- 2.3%). Myocyte apoptosis was patchy in distribution and was found predominantly in the subendocardial myocardium (9.8 +/- 4.6%) and rarely in the subepicardial myocardium (0.32 +/- 0.45%). Apoptosis was found not only around focal fibrosis areas, but also in areas without fibrosis or patchy infarction. Apoptosis was found not only in 24-h hypoperfused myocardium, but also in 4-week hypoperfused myocardium. The severity of myocyte apoptosis correlated significantly with regional coronary blood flow reduction (r = 0.75, p < 0.01). No apoptosis was found in the normal control region. CONCLUSIONS: This study demonstrates that there is ongoing myocyte death through myocyte apoptosis in hypoperfused hibernating myocardium.

Animals↗
PubMedDate not supplied

HL-91-technetium-99m: a new marker of viability in ischemic myocardium.

BACKGROUND: Technetium 99m-HL91 is a new hypoxia imaging agent that demonstrates increased uptake in ischemic, viable myocardium. This study was performed to determine whether HL91 is taken up by nonviable myocardium. METHODS: Twenty-three Krebs-Henseleit buffer-perfused, isolated rat hearts were studied. Tc-99m-HL91 300 microCi was infused over 10 minutes, followed by a 60-minute clearance. Myocardial activity was monitored by use of an NaI crystal. Four groups were studied: control (flow = 12 mL/min, n = 7), low flow (flow = 1 mL/min, n = 6), no flow/reflow (60 minutes no flow/60 minutes reflow before Tc-99m-HL91 infusion, flow = 12 mL/min, n = 5), and cyanide-treated (before Tc-99m-HL91 infusion, flow = 12 mL/min, n = 5). Injury was assessed by creatine kinase, transmission electron microscopy, and triphenyltetrazolium chloride. RESULTS: Control (no injury) and cyanide-treated (severe injury) hearts demonstrated low uptake (6.3+/-0.5 mean+/-SEM and 5.7+/-1.2 microCi, respectively) and low 60-minute retention (13.8%+/-2.2% and 13.7%+/-3.9%, respectively). Low-flow hearts (minimal injury) demonstrated markedly increased uptake (43.5+/-2.8 microCi, P < .01) and increased 60-minute retention (33.2%+/-2.9%, P < .01) compared with control. No-flow/reflow hearts (moderate injury) demonstrated intermediate uptake (8.7+/-0.5 microCi, P < .05 to control), although retention was not significantly different (18.9%+/-3.5%, P = ns). Severely and rapidly injured myocardium demonstrated Tc-99m-HL91 peak uptake and retention indistinguishable from normal. Moderately injured myocardium demonstrated uptake intermediate between severely injured and low-flow-induced ischemic, viable myocardium. CONCLUSION: Thus Tc-99m-HL91 is not taken up or retained in nonviable and irreversibly injured myocardium.

Animals↗
PubMed2004

Caloric restriction results in phospholipid depletion, membrane remodeling, and triacylglycerol accumulation in murine myocardium.

Herein, we utilize the power of shotgun lipidomics to demonstrate that modest caloric restriction results in phospholipid depletion, membrane remodeling, and triacylglycerol (TAG) accumulation in murine myocardium. After brief periods of fasting (4 and 12 h), substantial decreases occurred in the choline and ethanolamine glycerophospholipid pools in murine myocardium (collectively, a decrease of 39 nmol of phospholipid per milligram of protein at 12 h representing approximately 25% of total phospholipid mass and approximately 20 cal of Gibbs free energy per gram wet weight of tissue). Remarkably, the selective loss of long-chain polyunsaturated molecular species was present in the major phospholipid classes thereby altering the physical properties of myocardial membranes. No decrease in TAG mass was present in myocardium during fasting, but rather myocardial TAG increased during 12 h of refeeding nearly 3-fold returning to baseline levels only after 24 h of refeeding. No alterations in other examined lipid classes were present during fasting. In contrast to these lipid alterations in myocardium, no decreases in phospholipid mass were present in skeletal muscle myocytes and a dramatic decrease in skeletal muscle (or skeletal muscle associated) TAG mass was prominent after 12 h of fasting. These results identify phospholipids as a rapidly mobilizable energy source during modest caloric deprivation in murine myocardium, while triacylglycerols are a major source of energy reserve in skeletal muscle. Collectively, these results demonstrate dramatic alterations in the membrane composition of mildly fasted mammalian myocardium that identify the unanticipated plasticity of myocardial phospholipids to adapt to modest chemical and physical perturbations.

Animals↗
PubMed1998

Receptor occupancy in myocardium, adrenal cortex, and brain by TH-142177, a novel AT1 receptor antagonist in rats, in relation to its plasma concentration and hypotensive effect.

PURPOSE: To study the relationship between angiotensin II (AII) receptor occupancy ex vivo in tissues plasma concentration and hypotensive effect of a novel AII receptor antagonist, TH-142177 and losartan in rats. METHODS: At 2, 8 and 24 hr after oral administration of TH-142177 and losartan in rats, AII receptors in myocardium, adrenal cortex and cerebral cortex were determined by radioligand binding assay using [125I]Sar1,Ile8-AII. Plasma concentrations of both drugs and metabolite in rats were also measured using validated HPLC assays. Further, systolic blood pressure (SBP) in conscious renal hypertensive rats treated orally with TH-142177 and losartan were measured by using a tail cuff plethysmographic method. RESULTS: Oral administration of TH-142177 (1.8 and 5.5 micromol/kg) and losartan (6.5 and 21.7 micromol/kg) in rats brought about dose-dependent decreases in [125I]Sar1,Ile8-AII binding sites (Bmax) in myocardium and adrenal cortex. The extent of receptor occupancy by both drugs in adrenal cortex was maximal at 2 hr later but that in myocardium at 8 hr later. Further, the receptor occupancy was more sustained in myocardium than adrenal cortex. The ex vivo binding affinity of TH-142177 for AII receptors in these tissues was roughly three times higher than that of losartan. Also, cerebral cortical [125I]Sar1,Ile8-AII binding was significantly reduced by oral administration of losartan but not by TH-142177. The time course of AII receptor occupancy by both drugs in adrenal cortex appeared to be in parallel with that of their plasma concentrations, while the time course in myocardium correlated with that of their hypotensive effects rather than plasma concentrations. CONCLUSIONS: TH-142177 produced a relatively selective and sustained occupancy ex vivo of AII receptors in myocardium and adrenal cortex of rats with approximately three times greater potency than losartan. Its time course of myocardial receptor occupancy was in parallel with that of hypotensive effect rather than plasma concentration.

Adrenal Cortex↗
PubMed2001

Ultrastructural and molecular changes in the left and right ventricular myocardium associated with ascites syndrome in broiler chickens raised at low altitude.

The present study examines ultrastructural and molecular changes in ventricular myocardium associated with ascites cases in fast-growing broilers raised at low altitude. Extensive ultrastructural lesions were seen in the left and right ventricular myocardium of broilers with fulminant heart failure and ascites. Significant changes included lesions in the myofibril contractile apparatus, altered mitochondria, marked reduction in the myofibril component, and changes in the extracellular matrix (ECM) architecture. No lesions were observed in hearts of slow growing broilers, but mild to moderate changes (predominantly in the left ventriculum) were apparent in the hearts from some clinically normal, fast-growing broilers. SDS-PAGE profiles of washed myofibrils showed several distinctly different bands in preparations from left ventricular myocardium of ascitic birds. Western blot analysis of these samples revealed several fragments of myosin heavy chain, M-protein, and titin. Based on gelatinolytic activity, matrix metalloproteinases (MMP) in the cytosolic fraction of ventricular myocardium homogenates were identified as MMP-2. The relative activity of this enzyme appears to be considerably higher in preparations from broilers, particularly in the preparations from the left ventriculum of fast-growing broilers, in comparison to leghorns or slow growing broilers. The nature and distribution of the changes in the heart indicate that chronic cardiomyopathic process in the left ventricular myocardium occurs during the development of ascites. It is postulated that progressive deterioration of the left heart pump function caused by initial lesions in the left ventricular myocardium is a significant factor in the development of pulmonary hypertension and the pathogenesis of ascites in broilers raised at low altitude.

Altitude↗
PubMed2004

Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation.

INTRODUCTION: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. METHODS AND RESULTS: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. CONCLUSION: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart.

Animals↗
PubMed1993

Increased resistance against shortening in myocardium from recipient hearts of 7 patients transplanted for dilated cardiomyopathy.

UNLABELLED: The contractile behaviour of demembranized atrial and ventricular myocardium of 7 patients transplanted for end-stage heart failure (ESHF) was analyzed. Atrial muscle specimens of patients undergoing coronary artery bypass surgery (n = 9) and pig papillary muscle were used as reference preparations (n = 9). Extreme care was taken for dissection and mounting the muscle fibres (0.3 x 6 mm) in order to keep the passive series compliance small. Calcium sensitivity, cross-bridge cycling rate (estimated by the force-clamping technique and calculation of the shortening velocity at zero load [Vmax]) and isometric force development were measured. Analysis on light- and electronmicroscopic level was carried out. RESULTS: 1) Calcium sensitivity was not altered in ESHF patients; 2) the velocity of the force generating process (cross-bridge cycling rate) was normal in ventricular and reduced in atrial ESHF myocardium, 3) maximum isometric force development was reduced in ventricular, but not in atrial myocardium of ESHF patients, and 4) Vmax was significantly reduced in ventricular and atrial ESHF myocardium (p < 0.0001). Perimysial and endomysial fibrosis was present in ventricular, not in atrial myocardium of ESHF patients. CONCLUSION: A normal cross-bridge cycling rate in left-ventricular ESHF myocardium combined with a decreased capability of muscle shortening indicates the presence of a resistance against shortening localized either on the cross-bridge level or/and due to intra- and pericellular fibrosis. Left-ventricular contractile dysfunction in patients with end-stage heart failure may be related to a normal contractile apparatus contracting within an abnormal intracellular or interstitial environment.

Animals↗
PubMed1990

Quantitative ultrasonic assessment of normal and ischaemic myocardium with an acoustic microscope: relationship to integrated backscatter.

PURPOSE OF INVESTIGATION: The aim was to study ultrasonic propagation properties of normal and ischaemic myocardium with a scanning laser acoustic microscope and to correlate these changes with ultrasonic backscatter. DESIGN: Myocardial ischaemia was produced by total occlusion of left anterior descending coronary artery in anaesthetised open chest dogs. Myocardium supplied by left circumflex coronary artery served as normal control. IBR5, an optimum weighted frequency average (4-6.8 MHz) of the squared envelope of diffraction corrected backscatter, was measured in vivo. Ultrasonic attenuation coefficient, an index of loss per unit distance, the propagation speed and heterogeneity index were measured from normal and ischaemic regions with a scanning laser acoustic microscope which operates at 100MHz in vitro. Myocardial water content of normal and ischaemic myocardium was also estimated. SUBJECTS: Were five anaesthetised mongrel dogs. RESULTS: Attenuation coefficient of 33.8(SD4.2) dB.mm-1 in the ischaemic tissue was lower than 63.8(17.2) dB.mm-1 in the normal tissue (p less than 0.01). Ultrasonic speed was lower in ischaemic than normal myocardium at 1584(25) v 1612(35) m.s-1 (p less than 0.05). Heterogeneity index of 11(7) m.s-1 in the ischaemic region was lower than 14(8) m.s-1 in the normal region (27% reduction, p less than 0.05). IBR5 and myocardial water content were higher in the ischaemic than the normal myocardium: -37.2(SEM1.8) dB v -46.6(0.6) dB, (p less than 0.01) and 80.9(0.0)% v 78(0.2)%, (p less than 0.05) respectively. CONCLUSION: Ultrasonic properties of the myocardium are significantly altered during acute ischaemia.

Animals↗
PubMed1995

Adenosine technetium-99m sestamibi (SPECT) for the early assessment of jeopardized myocardium after acute myocardial infarction.

The purpose of this study was to evaluate the accuracy of adenosine Tc-99m sestamibi single photon emission computed tomography (SPECT) in the detection of jeopardized myocardium early after acute myocardial infarction. Coronary arteriography and myocardial scintigraphy were performed in 50 consecutive patients with an uncomplicated myocardial infarction. Myocardium was considered jeopardized if a significant infarct-related vessel stenosis (> 50% diameter stenosis) supplied an infarct area with residual viable tissue. Perfusion reversibility in the infarct region occurred in 25 patients (50%) and was almost solely observed in the presence of jeopardized myocardium. Non-reversible perfusion defects in the infarct region were found in patients without jeopardized myocardium. This subgroup consisted of either patients without significant vessel stenosis or patients without significant residual viability in the infarct region. Adenosine Tc-99m sestamibi SPECT had an accuracy of 88% for the detection of jeopardized myocardium. Side effects during adenosine infusion were frequently observed but well tolerated. These results suggest that adenosine Tc-99m sestamibi SPECT is an accurate non-invasive method for detecting jeopardized myocardium after acute myocardial infarction and may be a valuable non-invasive test for the early selection of patients at risk for future ischaemic events.

Adenosine↗