Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of propranolol on periinfarction block, myocardial ischemic injury and left ventricular performance following anterior descending coronary artery occlusion were studied. Experiments were made in 14 dogs anesthetized with pentobarbital sodium. Two minutes of reversible myocardial ischemia was induced by occlusion of descending left coronary artery. The severity of myocardial ischemia estimated by summing S-T segment elevation (sigma ST) from epicardial ECG mapping, heart rate, femoral arterial pressure and left ventricular (LV) dp/dt was determined before, during coronary occlusion alone and following propranolol infusion (0.25 mg/Kg) and coronary occlusion. Periinfarction block aspects on epicardial ECG appeared in four dogs following five repeated coronary occlusions. Propranolol infusion before coronary occlusion prevented the periinfarction block in every animal. The decrease of myocardial ischemia (sigma ST elevation), heart rate, arterial blood pressure and LV dp/dt following propranolol and coronary occlusion might be partly due to the beneficial effect of this drug on periinfarction block.
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PMID:Effect of propranolol on experimental periinfarction block and myocardial ischemia. 59 24

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76

Heparin has been labeled with [99mTc] pertechnetate and its ability to image damaged coronary vessels and myocardium during and following myocardial ischemia has been studied in experimental animals. The data obtained indicate that Tc-99m heparin localizes in damaged myocardium and coronary vessels in canine models of temporary myocardial ischemia and reperfusion and in damaged myocardium during fixed coronary occlusion. Scintigraphic detection of damaged myocardium was possible in both models, but the highest levels of Tc-99m heparin in damaged myocardial tissue were found in those dogs with temporary coronary occlusion and reflow. The data suggest that Tc-99m heparin may be of value as a positive imaging agent when coronary arteries or myocardium are injured and either reperfusion is allowed and/or significant blood flow persists in the damaged area.
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PMID:Technetium-labeled heparin: preliminary report of a new radiopharmaceutical with potential for imaging damaged coronary arteries and myocardium. 66 Feb 85

Myocardial ischemia has been associated with dispersion of ventricular refractory periods and this dispersion has been related to the ventricular arrhythmias seen with coronary occlusion. This study relates the degree of change in measured ventricular refractory period with the degree of regional myocardial blood flow abnormality after coronary occlusion. When regional myocardial blood flow is less than 70% of that of nonischemic areas, refractory periods are significantly (P less than 0.001) shortened. The greatest change in refractory periods occurs in areas with a regional myocardial blood flow that is 21 to 40% of that of nonischemic areas. Marked (less than 20%) and minimal (61 to 80%) reductions in regional myocardial blood flow are associated with less, but still significant, shortening of ventricular refractory periods. Thus dispersion of refractoriness can be related to the inhomogeneity of regional myocardial blood flow after acute coronary occlusion. Interventions designed to salvage ischemic myocardium by increasing regional myocardial blood flow may affect dispersion of ventricular refractory periods in complex and divergent ways.
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PMID:Relations between ventricular refractoriness and regional myocardial blood flow after acute coronary occlusion. 66 12

The relationship between progressive depletion of high energy phosphate and the onset of lethal cell injury in ischemic myocardium following coronary occlusion has been evaluated. Myocardial ischemia was induced by proximal occlusion of the circumflex coronary artery for 15, 30, 40, or 60 minutes. Cell injury in the severely ischemic posterior papillary muscle (PP) was evaluated by electron microscopy and by measuring the capacity of slices of the injured PP to maintain electrolytes, resynthesize high energy phosphate, and exclude inulin during in vitro incubation. ATP content in the ischemic myocardium decreased to 35%, 9%, 7%, and 5% of control values after 15, 30, 40, and 60 minutes of ischemia, respectively, and was associated with a corresponding depletion of total adenine nucleotides. The loss of 65% of the ATP after 15 minutes of ischemia (reversible injury) was associated with only minimal ultrastructural changes and no significant defects of electrolytes in incubated slices. However, the depletion of over 90% of the ATP after 40 minutes of ischemia (irreversible injury) was associated with significant fine structural changes and markedly altered cell volume regulation. The results suggest a close relationship between the marked depletion of high energy phsophates and the development of lethal injury in acutely ischemic myocardium.
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PMID:Relation between high energy phosphate and lethal injury in myocardial ischemia in the dog. 68 46

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.
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PMID:Changes in ventricular recovery properties during and after temporary coronary artery occlusion. 69 Dec 76

We studied the role of cardiopulmonary vagal afferents in the cardiovascular responses to coronary artery occlusion in conscious dogs with intact carotid sinuses and following functional denervation of the arterial baroreceptors. The contributions of vagal afferents were determined by cold blocking the vagi. In dogs with intact carotid sinuses, coronary artery occlusion produced small decreases in mean cardiac output and arterial pressure, whereas heart rate increased by 35 beats/min. In dogs with intact carotid sinuses, vagal cold block increased mean arterial pressure by 22 +/- 2 (mean +/- SE) mm Hg and heart rate by 90 +/- 6 beats/min. Mean cardiac output increased by 505 +/- 90 ml/min. With the exception of heart rate, responses to coronary occlusion during vagal cold block were similar to the occlusion response prior to vagal cold block. Furthermore, prior occlusion of the coronary artery did not significantly influence the responses to vagal cold block. After arterial baroreceptor denervation, coronary artery occlusion resulted in a substantially greater fall in systemic arterial pressure (-52 mm Hg as compared to -8 mm Hg, with intact carotid sinuses) and peripheral resistance decreased by -0.49 peripheral resistance units (PRU). Vagal cold block following denervation increased the arterial pressure by 49 +/- 10 mm Hg and peripheral resistance by 0.59 +/- 0.13 PRU. Both values were significantly greater than those observed during vagal cold block prior to denervation. In arterial baroreceptor-denervated dogs, vagal blockade significantly attenuated the response to coronary occlusion. Therefore, in conscious dogs, vagal afferents from cardiopulmonary receptors exert a significant inhibitory influence on the peripheral vascular tone. When the carotid sinuses are intact, this inhibitory influence appears to be marked during myocardial ischemia. In the absence of functional arterial baroreflexes, vagal afferent activity contributes to the depressor responses observed during ischemia.
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PMID:The circulatory influences of vagal afferents at rest and during coronary occlusion in conscious dogs. 70 45

The antiarrhythmic activity of amitriptyline, a tricyclic antidepressant, was evaluated in anesthetized dogs 24 h after coronary occlusion, during the period of spontaneous ventricular arrhythmias. In all experiments amitriptyline was administered i.v. in incremental doses of 0.3 mg/kg at 1 min intervals until a conversion to normal sinus rhythm was evident. Amitriptyline administration resulted in conversion of the ventricular arrhythmia to a normal sinus rhythm in 100% of the animals tested at a mean dose of 1.3 +/- 0.1 mg/kg. Smaller doses also resulted in a dose-related decrease in non-sinus nodal pacemaker activity. Lidocaine, when administered to the same group of animals, produced a reduction of ectopic pacemaker activity, but did not eliminate it at a cumulative dose of 2 mg/kg. Antiarrhythmic doses of amitriptyline did not produce significant changes in arterial blood pressure, cardiac output or electrocardiographic parameters associated with atrioventricular or intraventricular conduction. The results of this study suggest that at very low doses amitriptyline may be an effective antiarrhythmic agent in ventricular arrhythmias associated with myocardial ischemia.
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PMID:The antiarrhythmic action of amitriptyline on arrhythmias associated with myocardial infarction in dogs. 71 May

The effects of 30-, 60-, and 90-min occlusion of the left anterior descending coronary artery and 60-min reperfusion were studied on the left ventricular dP/dt, myocardial ultrastructure, and tissue as well as blood lactate levels in dogs. The dP/dt was depressed by the occlusion, and reperfusion instituted after 30 min resulted in full recovery whereas that after 90 min had an adverse effect. Varying degrees of ultrastructural damage were noted after 60 and 90 min of occlusion and this was further exaggerated by reperfusion. Coronary occlusion markedly increased lactate content of ischemic myocardium, and the same returned to normal upon reperfusion. Myocardial ischemia for 30 or 60 min did not affect net arterial lactate extraction by the heart, but ischemia for 90 min reversed net lactate extraction to net lactate production by the heart. Reperfusion after 30 min of occlusion significantly increased lactate extraction, but reperfusion after 60 and 90 min of ischemia significantly decreased net lactate extraction and increased net production, respectively. The results indicate that estimation of net lactate exchange across the heart can be of value in assessing the viability of myocardium following coronary bypass surgery.
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PMID:Arterio-venous difference in lactate levels in myocardial ischemia and reperfusion. 74 23

The ST segments of the electrocardiogram (ECG) become elevated within 20 to 30 seconds after the onset of acute coronary occlusion and, when persistent, such changes offer a possible indirect marker of the extent and severity of myocardial ischemic injury and of eventual cell death. When ST-segment elevation on the epicardial ECG is measured 15 minutes after an acute coronary occlusion in the dog, a general correlation exists with biochemical changes, regional myocardial blood flow, and myocardial electrolyte alterations measured at 15 minutes, although when an effort is made to correlate the degree of such alterations with the magnitude of the ST-segment change there is considerable scatter. On the other hand, when the ST-segment elevation at 15 minutes is correlated with myocardial blood flow, histologic changes, and creating phosphokinase (CPK) depletion 24 hours later, the correlation is good. Possible mechanisms underlying ST-segment elevation are discussed, and data are reviewed which indicate that the epicardial ECG my be relatively insentive to subendocardial injury; in the experimental setting this problem may be partially corrected by the use of intramyocardial ECG leads. The extension of direct epicardial ECG maps to precordial ST-segment mapping poses additional problems that include reduced sensitively, problems due to reciprocal changes in the ECG at the body surface, surface contact of the electrodes, pericarditis, and individual variability in the rate of spontaneous regression of ST-segment changes. Such mapping appears reliable only for infarctions of the anterior and lacteral wall. Further research is necessary on analysis of the QRS complex, and use of vector leads. Despite these problems experimental and clinical studies indicate that precordial electrocardiographic analysis may be useful for detecting acute changes in the severity of ischemic injury over relatively short periods of time (2 to 4 hours). This indirect measure clearly will require correlation with specific markers of ischemic damage, but with further improvements it seems likely that analysis of serial ECG changes will evolve into a valuable and reliable nonivasive clinical tool for characterizing myocardial ischemia and infarction.
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PMID:Electorcardiographic ST-segment analysis in the characterization of myocardial ischemia and infarction. 76 19


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