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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether or not the fall in coronary perfusion pressure after coronary occlusion is the cause of remote myocardial ischaemia, regional myocardial blood flow was measured using radiolabelled microspheres before and after left anterior descending (LAD) occlusion in the presence of a left circumflex artery stenosis in 22 anaesthetised dogs. Aortic pressure was maintained constant at the time of left anterior descending artery occlusion in 13 dogs (group 1) and proximal left circumflex artery pressure was held constant by a servocontrolled pump in nine dogs with a carotid artery-left circumflex artery shunt (group 2). Despite the maintenance of constant mean aortic pressure in group 1, remote posterior bed mean(SEM) endocardial flow fell from 0.69(0.05) to 0.43(0.07) ml.min-1.g-1 (p less than 0.05). In the dogs in which left atrial pressure rose to less than or equal to 9 mmHg after left anterior descending artery occlusion, remote bed endocardial flow did not fall significantly (0.66(0.07) to 0.56(0.11) ml.min-1.g-1; NS). In contrast, remote bed endocardial flow fell from 0.73(0.07) to 0.28(0.06) ml.min-1.g-1 (p less than 0.0001) after left anterior descending artery occlusion in the dogs in which left atrial pressure rose to greater than 9 mmHg. The fall in remote bed endocardial flow was prevented in group 2 dogs by maintaining proximal left circumflex artery pressure constant (0.95(0.08) to 0.86(0.09) ml.min-1.g-1; NS). An important mechanism for the development of remote myocardial ischaemia appears to be the fall in proximal coronary perfusion pressure at the time of coronary occlusion.
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PMID:Mechanism of remote myocardial ischaemia after coronary occlusion in open chest dogs. 322 52

The severity of ischaemia in the left ventricle from total coronary occlusion is modified by retrograde blood flow through collateral or overlapping vessels, but whether that is true for the right ventricle is not known. The consequences and extent of ischaemic damage from occlusion of the right coronary artery were studied in anaesthetised dogs. In group 1 (n = 9), the right coronary artery alone was occluded; in group 2 (n = 8), the right coronary artery and overlapping vessels from the left anterior descending and circumflex coronary arteries were occluded. Occlusion for 2 h caused right ventricular end diastolic pressure to increase by 2.8(SEM 0.4) mm Hg in group 1 (p less than 0.05) and by 1.9(0.5) mm Hg in group 2 (p less than 0.05). Fractional shortening in the ischaemic zone became akinetic in group 1: 12.0(1.4)% v 0.1(1.6)%; p less than 0.05; and dyskinetic in group 2: 12.1(2.1)% v -1.2(0.9)%; p less than 0.05. In both groups, fractional shortening remained depressed during the ensuing 2 h of reperfusion. The incidence of right ventricular free wall necrosis was 56% in group 1 but 100% in group 2 (p = 0.082). The area of necrosis, expressed as a percentage of the area at risk, was 13.9(6.6)% in group 1 in contrast to 66.9(4.5)% in group 2 (p less than 0.05). Both groups had equal involvement of the subendocardial and subepicardial layers. We conclude that ligating epicardial overlapping vessels in addition to the right coronary artery produces a larger area of right ventricular free wall necrosis.
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PMID:Do overlapping vessels protect against canine right ventricular infarction after right coronary artery occlusion? 325 21

The effects of the new thromboxane A2 (TXA2) synthetase inhibitor sodium 6-(2-[1-(1H)-imidazolyl]methyl-4,5-dihydrobenzo[b]thiophene)carboxylate (RS-5186), 10 mg/kg i.v., on infarct size, polymorphonuclear leukocytes (PMNs) infiltration, gross myocardial hemorrhage and ventricular arrhythmias were studied using a canine coronary occlusion (2 h)-reperfusion (5 h) model. Infarct size (IS) and risk area (RA) were determined by a dual staining technique. 60 min before coronary occlusion dogs were randomly assigned to either the RS-5186 treated group (n = 11) or the control group (n = 15). RS-5186 reduced infarct size (RS-5186: 26.3 +/- 2.4% of RA (mean +/- SEM) vs control: 50.7 +/- 5.9%, p less than 0.01), and also reduced the area of gross myocardial hemorrhage (RS-5186: 3.9 +/- 2.6% of IS vs control: 22.4 +/- 4.0%, p less than 0.01). The drug also decreased the intensity of PMNs infiltration into the infarcted area (p less than 0.05). However, RS-5186 had no significant influence on the incidence of ventricular arrhythmias. These results suggest that the new thromboxane A2 synthetase inhibitor RS-5186 might be useful in salvaging ischemic myocardium.
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PMID:Myocardial salvage by a novel thromboxane A2 synthetase inhibitor in a canine coronary occlusion-reperfusion model. 337 68

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.
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PMID:Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog. 344 Feb 62

The effects of nifedipine on coronary vasodilation were studied during reactive hyperaemia after a transient coronary occlusion and during active hyperaemia associated with graded treadmill exercise. Studies were performed in 10 chronically instrumented dogs in which left circumflex coronary artery flow was measured with an electromagnetic flowmeter and myocardial oxygen extraction was determined from indwelling aortic and coronary sinus catheters. Thirty minutes after administration of nifedipine (10 micrograms.kg-1 iv), when coronary blood flow, arterial pressure, and heart rate had returned to control values, the vasodilatation following a 10 s coronary occlusion was significantly blunted, so that reactive hyperaemia blood flow debt repayment (mean(SEM)) was reduced from 387(39)% during control conditions to 270(33)% after nifedipine (p less than 0.05). In contrast, nifedipine did not alter the coronary vasodilatation that occurred in response to graded treadmill exercise so that the increase in coronary blood flow during exercise was not different from the control response. Thus, although nifedipine blunted ischaemic coronary vasodilatation during reactive hyperaemia, it did not alter coronary vasodilatation during active hyperaemia resulting from physiological increases of myocardial oxygen consumption.
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PMID:Effects of nifedipine on coronary reactive and exercise induced hyperaemia. 344 Feb 69

To characterise collateral blood flow patterns after coronary artery occlusion in the rat and to determine whether tissue can be salvaged by reperfusion in this model, anaesthetised rats were subjected to 20, 30, 40, 60 min of coronary occlusion followed by 24 h of reperfusion or 24 h of permanent occlusion. Relative regional blood flow was measured by radioactive microspheres after 10 min of occlusion in rats undergoing 30 min of occlusion plus reperfusion and in those undergoing 24 h of permanent occlusion. The area at risk was determined by in vivo injection of fluorescent microspheres and necrosis delineated by in vitro tetrazolium staining. Tracings of heart slices were planimetered and the area of necrosis and transmural extent of the infarct measured. Blood flow in the area at risk during occlusion was similar in both the reperfused and permanent occlusion groups. In the 30 min group mean(SEM) subendocardial flow was reduced to 13(5)% of normal and subepicardial flow to 9(3)% and in the permanent occlusion group to 11(2)% and 8(3)% respectively. As delineated by fluorescent microspheres the area at risk was transmural in all rats; however, infarct size expressed as a percentage of the area at risk increased as the duration of occlusion increased. In rats reperfused up to 30 min after occlusion the area of necrosis as a percentage of the area at risk was significantly decreased compared with that in the permanent occlusion group (36.4(9.2)% in rats with 30 min occlusion plus 24 h reperfusion and 78.6(7.4)% in rats with permanent occlusion).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of early coronary artery reperfusion on infarct development in a model of low collateral flow. 344 71

The effect of a moderate increase in heart rate on regional blood flow (8-10 mu radiolabeled microspheres) to myocardium supplied by a stenosed left circumflex coronary artery with (n = 11) or without (n = 7) concomitant left anterior descending coronary artery occlusion was investigated in anesthetized mongrel dogs. In the presence of a left circumflex coronary artery stenosis (gradient 32 +/- 5 mmHg [x +/- SEM]) and an unstenosed left anterior descending coronary artery a pacing-induced rise in heart rate (22 +/- 1 beats/min) increased epicardial flow to the posterior wall supplied by the left circumflex coronary artery (+0.21 +/- 0.08 mL/min/g, p = 0.03). Posterior bed endocardial flow was unchanged (-0.03 +/- 0.08 mL/min/g, p = 0.76). In dogs with a left circumflex coronary artery stenosis of similar severity (gradient 34 +/- 4 mmHg), left anterior descending coronary occlusion did not significantly alter posterior bed endocardial or epicardial flow. Atrial pacing increased heart rate by 22 +/- 1 beats per minute and caused remote posterior bed endocardial flow to fall (-0.08 +/- 0.03 mL/min/g, p = 0.03). Epicardial flow to that region rose (+0.09 +/- 0.02 mL/min/g, p less than 0.0002). Thus, a moderately severe coronary stenosis prevents the expected increase in endocardial flow normally seen after an increase in heart rate. Remote bed endocardial flow actually falls when heart rate is increased in the presence of an occlusion in a second major coronary artery.
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PMID:The effect of an increase in heart rate on remote myocardial blood flow in a two vessel coronary stenosis-occlusion model. 359 95

We have examined the temporal response of regional subendocardial function in conscious chronically instrumented dogs following implantation of a circumflex ameroid occluder. Collateralization was limited by ligation of epicardial anastamoses between the circumflex and adjacent coronary arteries at the time of instrumentation. Sonomicrometrically measured regional function in the circumflex coronary artery became depressed relative to that in the left anterior descending coronary artery bed under resting conditions with the onset of an aortic-circumflex pressure gradient of 15 +/- 2.9 mm Hg (mean +/- SEM). At the time of total ameroid occlusion, the ratio of circumflex to left anterior descending coronary artery function fell to 68 +/- 8% of control, with mean circumflex coronary pressure decreasing to 60 +/- 1.6 mm Hg. Following ameroid occlusion, distal coronary pressure increased, and circumflex function recovered towards control but remained depressed relative to that in the left anterior descending coronary artery for 2-4 weeks. Measurements of regional subendocardial perfusion suggested a dissociation between subendocardial flow and function prior to but not following coronary occlusion by the ameroid. We conclude that this model results in reductions in regional function that are relatively prolonged and are not readily attributable to subendocardial infarction or a critical reduction in resting coronary flow. The data suggest that functional adaptations in response to gradually developing coronary occlusion are more complex than those associated with acute reductions in coronary artery pressure and flow.
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PMID:Reductions in regional myocardial function at rest in conscious dogs with chronically reduced regional coronary artery pressure. 366 82

To evaluate the effect of an assist pump on the metabolic viability of the ischemic myocardium, myocardial pH was continuously monitored using an ion-sensitive field-effect transistor (ISFET) pH sensor in 14 dogs after coronary occlusion. In seven dogs (control group), coronary occlusion (10-20 min) and successive reperfusion (30-60 min) were performed several times. In seven dogs [left ventricular assist device (LVAD) group], the LVAD was implanted between the left atrium and the aorta. Occlusion and reperfusion were performed first with the pump on and then with the pump off. In both groups, myocardial pH fell after occlusion, and increased after reperfusion. In the control group, the fall rate of pH in the later coronary occlusion decreased to 66 +/- 7% (mean +/- SEM) of that in the previous occlusion. Contrarily, in the LVAD group, the fall rate under LVAD-off increased to 174 +/- 32% of that under the preceding LVAD-on. This indicates that progressive cellular damage occurred in the control group, while the myocardium was preserved by the assist pump in the LVAD group. LVAD is effective for preserving the metabolic viability of the ischemic myocardium.
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PMID:Effect of left ventricular assist device (LVAD) on myocardial pH change after regional coronary occlusion. 368 75

The effects on myocardial damage of metabolic interventions by nicotinic acid, oxfenicine, or a combination of the two were assessed in open-chest dogs exposed to coronary artery occlusion for 6 hours. The accumulation of metabolites of free fatty acids (FFAs) was studied in tissue samples of the left ventricle taken 60 minutes after coronary occlusion in separate animals. The percentage of the hypoperfused zone that evolved to infarction was 96 +/- 3% (mean +/- SEM) in control dogs, 74 +/- 4% in dogs treated with nicotinic acid (p less than 0.05 vs control dogs), 72 +/- 2% in dogs treated with oxfenicine (p less than 0.05 vs control dogs), and 54 +/- 5% in dogs with combined nicotinic acid and oxfenicine (p less than 0.05 vs control dogs, p less than 0.05 vs nicotinic acid and oxfenicine). Arterial FFA concentration was markedly reduced in dogs treated with nicotinic acid and those treated with combination nicotinic acid and oxfenicine. The accumulation of long-chain acyl carnitine was substantially reduced in the ischemic myocardium after nicotinic acid, oxfenicine, and a combination of the two, whereas the lowering of long-chain acyl CoA was less pronounced. Thus, nicotinic acid and oxfenicine, which depress myocardial FFA metabolism by different mechanisms, both reduce myocardial infarct size and their effects are additive.
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PMID:Limitation of myocardial infarct size by metabolic interventions that reduce accumulation of fatty acid metabolites in ischemic myocardium. 371 78


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