Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether nifedipine, a calcium antagonist, protects ischemic myocardium, conscious dogs were subjected to coronary occlusion and given nifedipine by intravenous infusion beginning 30 minutes after the onset of ischemia and lasting for 24 hours while systemic arterial pressure, left atrial pressure, and cardiac output were monitored. Local myocardial perfusion at selected intervals after coronary occlusion was assessed with radioactive microspheres injected into the left atrium. In regions of myocardium exhibiting moderately depressed flow 29 minutes after occlusion in control dogs (n = 8), flow was significantly greater 3 and 23.5 hours later, reflecting increases in collateral perfusion. Corresponding zones of myocardium in treated dogs (n = 9) exhibited significantly greater increases in flow at each interval after occlusion (P less than 0.05). Furthermore, myocardial creatine kinase depletion (which correlated well with morphometric estimates of necrosis) in myocardium matched for ischemia prior to treatment was 1.5 to 3 times less in treated than in control dogs (P less than 0.05). Thus, nifedipine produced sustained increases in collateral flow and reduced myocardial ischemic injury.
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PMID:Effects of nifedipine on myocardial perfusion and ischemic injury in dogs. 67 20

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.
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PMID:Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion. 68 53

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 purpose of this study was to determine the relative magnitudes of the reflex effects mediated by cardiac receptors during anterior as opposed to inferoposterior ischemia of the left ventricle of the dog. Cessation of perfusion (coronary "occlusion") of the circumflex coronary artery (Cx) in 29 chloralose-anesthetized dogs with common carotids ligated (group I) resulted in significant bradycardia and hypotension, but in no significant change in perfusion pressure in the gracilis muscle perfused at constant flow. Occlusion of the left anterior descending coronary artery (LAD) produced less hypotension, no change in heart rate, and vasoconstriction in the gracilis. After vagotomy and aortic nerve section, no significant change in heart rate or gracilis perfusion pressure was observed during lad or Cx occlusion, and the blood pressure responses to LAD and Cx occlusion were not different. In nine dogs with sinoaortic denervation (group II), brief Cx occlusion resulted in bradycardia, hypotension, and vasodilation in the gracilis muscle. LAD occlusion in group II dogs caused less hypotension and no change in heart rate or gracilis perfusion pressure. After vagotomy, the bradycardia and vasodilation resulting from Cx occlusion were abolished and the blood pressure responses to LAD and Cx occlusion were not different. The weights of left ventricle perfused by each occluded vessel were not different. These data show that left ventricular receptors with vagal afferents which are activated during coronary occlusion and which mediate cardioinhibitory and vasodepressor responses are located mainly in the inferoposterior left ventricle of the dog heart.
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PMID:Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog. 68 55

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 solid angle theory has long been applied to the interpretation of the ECG; however, quantitative evaluation of its applicability has been minimal. We applied solid angle analysis to the interpretation of the TQ-ST deflection during acute ischemia. Five anesthetized pigs were studied 1--3 hours after coronary occlusion. Multiple unipolar tracings were recorded from precisely determined positions on the epicardium overlying the ischemic and normal zones. The geometry of the hearts and ischemic zones was preserved, the margins of ischemia being defined as the outer border of Thioflavin S nonfluorescence. Wax replicas of the hearts with ischemic zones removed were constructed. Solid angles subtended at electrode positions on the replicas were calculated. A linear relationship (r = 0.84 - 0.97, P less than 0.001) was shown to exist between the observed TQ-ST deflection and the calculated solid angle. A small but patterned deviation from exact fit of the TQ-ST deflection with the calculated solid angle led us to investigate the possibility that dipole moment strength (phi) is not confined to the ischemic margins. Computations using idealized heart models with ischemic zones cylindrical and transmural in shape allowed us to distribute phi arbitrarily within the ischemic zone, comparing this predicted pattern of TQ-ST deflection with that observed experimentally. The experimental data appear most consistent with the condition in which phi is distributed over a 1-cm border region during the first several hours of ischemia. We conclude that the solid angle theory provides a rational basis for interpretation of the ischemic TQ-ST deflection; however, phi may be distributed over a marginal zone.
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PMID:A solid angle analysis of the epicardial ischemic TQ-ST deflection in the pig. A theoretical and experimental study. 70 50

The influence of an instantaneous increase in afterload on the hemodynamics and regional myocardial function was studied in five anesthetized dogs before and after occlusion of the left anterior descending coronary artery. By inflation of an intaaortic balloon during single ejections, an instantaneous increase in afterload was obtained. From biplane cineventriculograms, the following parameters were calculated: left ventricular volumes (EDV, ESV), stroke volume (SV), ejection fraction (EF). Mean circumferential fiber shortening (V CF) was calculated in three ventricular diameters in the RAO projection. Simultaneously PLV, PLVED, PAo, and LV dp/dt were obtained. In the control ventriculograms, an increased afterload (delta PLV 16.4 +/- 8 mm Hg) caused only a minor decrease of SV (2.6 +/- 2.5 ml), EF (4.2 +/- 2.4%), and V CF (0.20 circ . s -1). After coronary occlusion (delta PLV 14.5 +/- 6.7 mm Hg),the reduction of SV (5.9 +/- 2.7 ml) and EF (8.2 +/- 2.6%) was more pronounced. This was caused mainly by a significant reduction of V CF in the center of ischemia (delta V CF -93%). For the evaluation of regional myocardial function by ventriculography, the marked influence of afterload in ischemic areas must be taken into consideration. This is of special interest in comparative ventriculograms, such as those before and after coronary bypass surgery.
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PMID:[The influence of afterload on the normal and ischemic myocardium in the dog]. 71 34

In a complex experimental study on 52 dogs the myocardium was examined after ischemia and reperfusion of various duration. Morphologic, metabolic, and functional findings proved that a short-term reperfusion after coronary occlusion for more than 2 hours has disadvantageous effects on the regression of ischemic lesions. During the early period (up to 3 days) this is caused by the "no-reflow" phenomenon. Combined qualitative and quantitative findings are required for correct appraisal of the ultrastructural alterations after reperfusion. In acute coronary occlusion, early revascularization after passing the crucial initial phase is advantageous, because the extent of myocardia necrosis is decreased by the prolonged reperfusion, thus leaving a larger myocardiac reserve in case of re-infarction. Clinical conclusions are drawn.
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PMID:[Reperfusion of the myocardium after acute ischemic lesion]. 73 61

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

Subendocardial ischemia during coronary occlusion in dogs was studied using S-T segment elevations in unipolar subendocardial electrodes. Alterations in heart rate or cardiac output caused quantitatively similar changes in subendocardial and epicardial S-T elevation. Increasing blood pressure from 75 to 100 or 75 to 125 mm Hg caused a smaller reduction in subendocardial than in epicardial S-T elevation (p less than 0.01). In this situation, therefore, subendocardial ischemia tends to be maintained while epicardial ischemia is reduced by higher arterial pressures. Hemodynamic manipulations can cause quantitatively different changes in subendocardial and epicardial S-T segment elevation.
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PMID:Subendocardial S-T segment changes during acute coronary occlusion. 80 58


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