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)

Occlusion of the anterior descending coronary artery was produced in sedated baboons 7-15 days after implantation of a micromanometer and ultrasonic crystals for measurement of regional left ventricular dimensions in ischemic, marginal, and control segments. One minute after coronary occlusion (CO), ischemic segments exhibited a marked systolic bulge with wall thinning, and percent systolic shortening of marginal segments decreased. Over the ensuing weeks, there was a progressive increase of end-diastolic lengths in marginal and ischemic segments, whereas systolic shortening in these segments did not improve significantly. Control segments did not change. In control baboons, the coronary collateral index was 55 +/-25 (SE) compared to 560 +/- 74 in normal dogs. One month after CO, the collateral index was 543 +/- 144 in baboons compared to 6,685 +/- 716 in dogs, regions of normal tissue were seen in the infarct (14.2 +/- 2% of left ventricular mass). Minimal coronary collateral development in the baboon provides a likely explanation for differences from the dog in regional functional responses and in the character of the infarct.
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PMID:Myocardial infarction in the baboon: regional function and the collateral circulation. 10 19

Isolated perfused hearts from rats acclimatized to Jungfraujoch (altitude 3454 m) were less resistant to the effects of high levels of heart work or mild hypoxia than hearts from litter mates reared at Geneva (340 m). However, in response to coronary artery ligation hearts from acclimatized rats were better able to maintain tissue contents of adenosine triphosphate, phosphocreatine and glycogen. A projected explanation for the increased biochemical resistance to ischaemia was a relative increase in the coronary flow rate. The data support the hypothesis that exposure to high altitude helps to protect the heart against coronary occlusion by an increased resistance developing as a result of increased sensitivity to high levels of heart work and hypoxia.
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PMID:Effects of increased left ventricular work, hypoxia, or coronary ligation on hearts from rats at high altitude. 10 23

The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.
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PMID:Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion. 10 8

The purposes of this study were to demonstrate that echocardiography can be used to demonstrate the systolic wall thinning of acutely ischemic myocardium, and to compare the effects of nitroglycerin and nitroprusside on systolic thinning, wall stress and perfusion of ischemic myocardium. In 37 dogs, the ratio of end-systolic-to-end-diastolic posterior wall thickness fell from 1.30 +/- 0.02 to 0.88 +/- 0.01 ((p less than 0.001) after circumflex coronary occlusion; perfusion of the area supplied by the occluded artery fell from 98.2 +/- 7.5 ml/100 g/min to 36.5 +/- 2.9 ml/100 g/min (p less than 0.001). Nitroglycerin and nitroprusside were given to lower mean arterial pressure by 7% and 15%. Despite the reduction in coronary perfusion pressure, transmural perfusion, endocardial/epicardial perfusion ratio and systolic thinning remained constant. Both drugs reduced the ischemic "wall stress index" (ventricular pressure x ventricular diameter/wall thickness) by almost 50%. Thus, both nitroglycerin and nitroprusside were equally beneficial in this model of acute myocardial ischemia.
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PMID:Effect of acute ischemia, nitroglycerin and nitroprusside on regional myocardial thickening, stress and perfusion. Experimental echocardiographic studies. 10 33

The amplitude and distribution of epicardial ST-segment elevation (ST) were examined for an 8-hour period after coronary occlusion in eight baboons and five pigs. ST was determined from unipolar epicardial electrograms obtained from a high-resolution matrix of fixed electrodes overlying a transmural region of ischemia. A relatively uniform degree of ST was observed overlying the ischemic region for 20 minutes after coronary occlusion. A gradient in ST from the periphery to the center of the ischemic region was documented after 20 minutes of ischemia. In 10 other pigs, change in the degree of ST was examined contingent on either an increase (five pigs) or decrease (five pigs) in the size of the ischemic region after 1 hour of preexisting ischemia. An abrupt increase in the number of electrodes that showed ST (NST) from 7.8 +/- 1.24 (SEM) to 14.8 +/- 1.35 (90%) was associated with an increase in mean ST of 58% from 4.28 +/- 0.61 mV to 6.78 +/- 0.84 (p less than 0.05). An abrupt decrease in NST from 25.2 +/- 2.63 to 14.6 +/- 2.22 (42%) was associated with a decrease in mean ST of 24%, from 8.2 +/- 0.36 mV to 6.3 +/- 0.30 mV (p less than 0.01). The results during early ischemia (less than 20 minutes of ischemia) are accurately represented by a model of ischemia in which injury current arises only at the ischemic boundary. The results during later ischemia (after 20 minutes of ischemia) may be represented by a model in which ST is considered dependent on injury currents generated throughout the ischemic region.
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PMID:Epicardial mapping and electrocardiographic models of myocardial ischemic injury. 11 30

Nitroglycerin is known to affect the electrophysiological properties of the ischaemic ventricle, possibly by altering regional myocardial blood flow. This study correlated the effects of nitroglycerin, given after acute coronary occlusion, on regional ventricular refractoriness and regional myocardial blood flow. Nitroglycerin returned ventricular refractory periods to their pre-occlusion values in spite of no significant effect on regional myocardial blood flow. Although the beneficial electrophysiological effects of nitroglycerin were not explained by increased regional flow to the ischaemic myocardium, an improved myocardial oxygen supply-demand balance may have produced these favourable effects. This study emphasises the need for electrophysiological evaluation of the effects of interventions intended to limit infarct size.
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PMID:Dissociation of effects of nitroglycerin on regional refractoriness and regional myocardial blood flow following acute coronary occlusion. 11 1

The left anterior descending coronary artery was ligated in 6 baboons. Subsequently, 3 animals were supported with long-term (24-hour) intraaortic balloon pumping (IABP), and 3 were on coronary occlusion alone. Animals were studied hemodynamically and with unipolar electrocardiographic mapping acutely and then were studied after a week and killed. A histological measurement of infarct size was made. The use of IABP had no influence on the area of ischemia determined by unipolar mapping or on infarct size measured quantitatively at a week. Similarly, there were no acute hemodynamic differences between the two groups. The only significant difference noted was a reduction in systolic pressure in IABP animals during balloon pumping and a significantly higher left ventricular systolic pressure a week following infarction in animals treated with IABP. The data indicate no significant effect of IABP on altering infarct size in animals with acute coronary ligation in the absence of cardiogenic shock.
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PMID:The effects of intraaortic balloon counterpulsation on myocardial infarct size. 11 7

The aim of the study was to investigate whether the beta blocking agent, practolol, is able to modify some of the metabolic and hormonal responses and the local myocardial changes evoked by an excess of adrenaline similar to that seen after acute coronary occlusion. Adrenaline (1.2 micrograms/kg/min) and practolol (1 mg/kg) were infused concurrently to anaesthetized intact dogs for 5 h. Blood free fatty acid and triiodothyronine levels were measured initially and after 2, 4 and 5 h of infusion. At the end of the infusion the myocardium was subjected to biochemical, histoenzymatic and electron microscopic examination. The results were compared with those obtained in dogs infused with adrenaline alone and with saline alone. Practolol reduced the adrenaline-induced increase in free fatty acids and a fall in triiodothyronine in the blood. Myocardial acetate accumulation and ATP decrease were both reduced by practolol. Histoenzymatic and electron microscopic changes were less. These effects of practolol upon systemic and myocardial disturbances induced by the excess of adrenaline indicate that it might be effective in modifying any excessive adrenergic response which may occur in acute myocardial infarction.
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PMID:Beneficial effect of practolol in preventing adrenaline-induced systemic and myocardial metabolic changes. 11 21

This study shows that noncoronary collateral flow occurs in normal hearts after chronic coronary occlusion and with left ventricular hypertrophy in variable amounts (0.2 to 16 ml/100 gm/min). Luminal--left ventricular flow is greatest when the heart is arrested by aortic cross-clamping, falls significantly when perfusion pressure is lowered to 50 mm Hg, and increases slightly when blood viscosity is reduced (hemodilution). Our findings indicate that the heart which is arrested by aortic cross-clamping may not be anoxic.
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PMID:Noncoronary collateral myocardial blood flow. 12 34

The effects of ischemia on the canine myocardial (Na+ + K+)-ATPase complex were examined in terms of alterations in cardiac glycoside binding and enzymatic activity. Ability of the myocardial cell to bind tritiated ouabain in vivo was assessed after 1, 2, and 6 h of coronary occlusion followed by 45 min of reperfusion, and correlated with measurements of in vitro (Na+ + K+)-ATPase activity and in vitro [3H]ouabain binding after similar periods of ischemia. Regional blood flow alterations during occlusion and reperfusion were simultaneously determined utilizing 15 mum radioactive microspheres to determine the degree to which altered binding of ouabain might be flow related. Anterior wall infarction was produced in 34 dogs by snaring of confluent branches of the left coronary system. Epicardial electrograms delineated ischemic and border zone areas. Coronary reperfusion after 2 and 6 h of occlusion was associated with impaired reflow of blood and markedly impaired uptake of [3H]ouabain in ischemic myocardium. In both groups, in vivo [3H]ouabain binding by ischemic tissue was reduced out of proportion to the reduction in flow. Despite near-complete restoration of flow in seven dogs occluded for 1 h and reperfused, [3H]ouabain remained significantly reduced to 58 +/- 9% of nonischemic uptake in subendocardial layers of the central zone of ischemia. Thus, when coronary flow was restored to areas of myocardium rendered acutely ischemia for 1 or more hours, ischemic zones demonstrated progressively diminished ability to bind ouabain. To determine whether ischemia-induced alteration in myocardial (Na+ + K+)-ATPase might underlie these changes, (Na+ + K+)-ATPase activity and [3H]ouabain binding were measured in microsomal fractions from ischemic myocardium after 1, 2, and 6 h of coronary occlusion. In animals occluded for 6 h, (Na+ + K+)-ATPase activity was significantly reduced by 40% in epicardial and by 35% in endocardial layers compared with nonischemic myocardium. Comparable reductions in in vitro [3H]ouabain binding were also demonstrated. Reperfusion for 45 min after occlusion for 6 h resulted in no significant restoration of enzyme activity when compared to the nonreperfused animals. In six animals occluded for 2 h, a time at which myocardial creatine phosphokinase activity remains unchanged, (Na+ + K+)-ATPase activity was reduced by 25% compared with nonischemic enzyme activity. In five dogs occluded for 1 h, (Na+ + K+)-ATPase activity in ischemic myocardium was unchanged from control levels. We conclude that reduced regional myocardial blood flow, local alterations in cellular milieu, and altered glycoside-binding properties of (Na+ + K+)-ATPase all participate in the reduction of cardiac glycoside binding observed after reperfusion of ischemic myocardium. In addition, after 2 or more hours of severe ischemia, myocardial (Na+ + K+)-ATPase catalytic activity is significantly reduced despite incubation in the presence of optimal substrate concentrations.
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PMID:Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding. 13 Mar 83


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