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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The functional significance of the coronary collateral circulation remains controversial. It has been suggested that collateral circulation possibly helps prevent myocardial ischemia. Seventeen target lesions in 15 patients were studied to determine the relationship between the extent of the coronary collateral circulation and the degree of ventricular dysfunction during percutaneous transluminal coronary angioplasty (PTCA). During the first balloon inflation, diastolic indices such as left ventricular end-diastolic pressure, max negative dP/dt and the time constant of early relaxation were measured immediately before and at 60 sec following balloon inflation. During the second inflation, the contralateral and ipsilateral collateral circulations were evaluated. The latter was graded as follows: 0 = none; I = filling of side branches only; II = partial filling of the epicardial segment; and III = complete filling of the epicardial segment. Following balloon inflation, a significant increase was noted in the time constant of early relaxation in patients with grade 0 collateral circulation (40 +/- 7 to 47 +/- 7 msec: p < 0.01) and grade II collateral circulation (52 +/- 12 to 56 +/- 13 msec: p < 0.05). The percent increase in the time constant of early relaxation of patients with grade 0 and I collateral circulations exceeded that of patients with grade II (p < 0.05) or grade III collateral circulation (p < 0.05). Left ventricular end-diastolic pressure was elevated in all groups during PTCA. There was no significant difference in the percent increase of left ventricular end-diastolic pressure (LVEDP) between the 4 groups. However, LVEDP before PTCA was higher in patients with grade III collateral circulation than in patients in the other groups. Max negative dP/dt did not change significantly in any group. In conclusion, collateral circulation helps prevent myocardial ischemia during acute coronary occlusion, which is most precisely shown by the time constant of early relaxation. The degree of this protective function of collateral circulation seems to vary.
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PMID:[The functional significance of coronary collateral circulation during sudden coronary occlusion]. 134 23

Myocardial ischemia followed by reperfusion was produced in artificially respirated, open-chest rats. Coronary artery ligation for 6 min rarely evoked arrhythmias; however, reperfusion after this period rapidly produced severe dysrhythmias in all control animals. Reperfusion after 12 min of ischemia produced less frequent dysrhythmias than after coronary occlusion for 6 min. Feeding of a linoleic acid-rich diet, applying 12% sunflower seed oil in rat food pellet for 4 weeks, decreased the incidence of reperfusion-induced ventricular fibrillation both after 6 min (2/15 vs. 7/11) and 12 min (0/11 vs. 2/8) of myocardial ischemia and the incidence of other arrhythmias was also decreased. The number of animals developing no arrhythmias during reperfusion was increased (8/15 after 6 min of ischemia, 4/11 after 12 min of ischemia vs. 0/11 and 0/8 in controls, respectively). Our results indicate that increased dietary consumption of linoleic acid decreased the occurrence of life-threatening arrhythmias both during the acute phase of myocardial ischemia and during reperfusion in anesthetized rats.
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PMID:Effect of dietary sunflower seed oil on the severity of reperfusion-induced arrhythmias in anesthetized rats. 137 86

The purpose of this study was to determine whether the selective type IV cAMP-phosphodiesterase inhibitor rolipram could reduce the reperfusion injury that occurs during myocardial infarction in the anesthetized dog. This question was tested in pentobarbital-anesthetized dogs subject to 90 min of regional myocardial ischemia and 5 h of reperfusion. Dogs were treated with 1 mg/kg of rolipram (i.v., 15 min before reperfusion) followed by a 1 mg/kg/h infusion over the duration of the 5 h of reperfusion. Rolipram was tested in vitro for efficacy in inhibition of isolated human neutrophil superoxide generation. Rolipram produced significant inhibition of superoxide production over the concentration range of 0.1-100 microM rolipram when neutrophils were stimulated with a 10(-7) M concentration of the chemotactic peptide f-Met-Leu-Phe. Rolipram significantly inhibited superoxide generation from human and canine granulocytes in whole blood stimulated by zymosan. Therapeutic concentrations of rolipram in the blood of dogs were achieved during the course of the experiments with a plasma concentration of 0.761 +/- 0.095 micrograms/ml (2.76 +/- 0.34 microM) at the time of reperfusion, and 0.574 +/- 0.098 micrograms/ml (2.08 +/- 0.36 microM) at the end of the reperfusion period. The relative severity of myocardial ischemia between the two treatment groups was similar as assessed with radiolabeled microsphere measurement of myocardial blood flow. Transmural myocardial blood flows were not significantly different between the two groups after coronary occlusion (control, 0.05 +/- 0.01 ml/min/g, n = 6, vs. rolipram, 0.18 +/- 0.07 ml/min/g, n = 6; p = 0.48).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of granulocyte cAMP-phosphodiesterase by rolipram in vivo is not sufficient to protect the canine myocardium from reperfusion injury. 137 23

The effects of decreasing blood viscosity by normovolemic hemodilution with dextran-40 or normal saline (NS) on myocardial lipid peroxides, superoxide dismutase, infarct size and left ventricular function during acute myocardial ischemia/reperfusion were studied in rabbits. It was found that normovolemic hemodilution with dextran-40 could decrease the content of ischemic myocardial malondialdehyde and preserve ischemic myocardial superoxide dismutase activity after 1 h of coronary occlusion followed by 1 h of reperfusion. However, after administration of NS only a tendency in this aspect exhibited without statistical significance. Besides, hemodilution with dextran-40 reduced infarct size and improved left ventricular systolic function after 1 h of ischemia followed by 23 h of reperfusion. These results suggest that normovolemic hemodilution with dextran-40 may have anti-injury effect on acute myocardial ischemia/reperfusion to a certain degree.
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PMID:The effects of normovolemic hemodilution with dextran-40 on acute myocardial ischemia/reperfusion injury in rabbits. 137 54

Previous results on the effects of angiotensin-converting enzyme (ACE) inhibition in myocardial ischemia are conflicting. To determine whether acute ACE inhibition may influence myocardial perfusion deficit during ischemia and reduce ischemia-reperfusion injury, anesthetized open-chest dogs underwent 2-h left anterior descending coronary artery (LAD) occlusion followed by 6-h reperfusion. After 1-h coronary occlusion, each dog was randomized to receive either captopril [5 mg/kg intravenous (i.v.) bolus and 0.25/kg/h infusion for 7 h] or saline. Whereas arterial pressure was reduced (p = 0.001), captopril did not influence myocardial perfusion deficit: Blood flow in the central ischemic zone represented 17.1 +/- 2.8% of the flow in the nonischemic zone versus 20.5 +/- 3.8% before treatment (NS). The values of the control group were 17.8 +/- 2.5 and 16.7 +/- 2.4%, respectively. In addition, there was no difference in infarct size: 35.9 +/- 3.3% of the area at risk in captopril-treated dogs versus 40.0 +/- 3.6% in controls. Analysis of subgroups based on the level of the collateral flow indicated, however, that ACE inhibition had an adverse effect on infarct size in dogs with high collateral flow: 31.9 +/- 4.6% in captopril dogs versus 17.6 +/- 4.7 (p = 0.048). This effect was related to a decrease in collateral flow because animals exhibiting the highest increase in perfusion deficit presented the greatest increase in infarct size (r = -0.92, p = 0.003). Although in dogs with low collateral flow, ACE inhibition appeared to exert a slight beneficial effect on infarct size, we conclude that at least in this dog model, acute ACE inhibition could exacerbate myocardial injury.
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PMID:Importance of the flow perfusion deficit in the response to captopril in experimental myocardial infarction. 137 9

Angiography in patients with unstable angina or myocardial infarction with subtotal coronary occlusion often reveals eccentric stenoses with irregular borders, suggesting ruptured atherosclerotic plaques and thrombosis, as documented by angioscopy and at autopsy. We have simulated and studied these processes in an ex vivo perfusion chamber and in an in vivo swine model. Our results suggest that specific local factors at the time of plaque disruption influence the degree of thrombogenicity, the stability of the growing thrombus, and, therefore, possibly also the various clinical syndromes. These factors can be divided into two groups: local vessel wall-related factors and systemic factors with local action at the area of risk. These factors include the following. 1) Exposed substrate-related effects: Plaque rupture produces a rough surface and stimulates the development of occlusive thrombus in proportion to the degree of damage. 2) Fluid dynamics-related factors: The more severe the stenotic lesion after plaque rupture, the higher the local shear rate, resulting in enhanced platelet deposition and thrombus formation. 3) Vasoconstrictive effects: Vasospasm is an important contributor to the pathogenesis of ischemic heart disease. 4) Systemic factors: There is clinical and experimental evidence to suggest that various systemic factors at the time of plaque rupture may enhance thrombogenicity (i.e., levels of epinephrine, levels of serum cholesterol, impaired fibrinolysis). We have investigated the role of residual thrombus on the process of rethrombosis and found that a residual thrombus is a very thrombogenic surface that may significantly contribute to reocclusion even in heparinized blood. Using recombinant hirudin as a pharmacological tool in our flow studies, we observed that rethrombosis is partially caused by thrombin bound to fibrin in the original thrombus, because the effect is abolished by the specific thrombin inhibitor.
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PMID:Thrombus formation on ruptured atherosclerotic plaques and rethrombosis on evolving thrombi. 142 53

A simple model of coronary occlusion and reperfusion in conscious rat was used to test the effects of various drugs on the arrhythmias. Blood pressure and ECG were monitored on a Grass polygraph. Intravenous infusion of test agents started before coronary occlusion and continued through the periods of occlusion and reperfusion. The free radical scavengers (allopurinol 12.3 mg/kg, mannitol 33.0 mg/kg, N-2-mercapto-propionyl glycine 8.6 mg/kg and adenosine 10.0 mg/kg), class 1-4 antiarrhythmic drugs (lidocaine 10.2 mg/kg, quinidine 12.3 mg/kg, propranolol 4.9 mg/kg, amiodarone 5.6 mg/kg and verapamil 1.1 mg/kg), aspirin 24.5 mg/kg and benadryl 3.7 mg/kg reduced the incidence of ventricular fibrillation and shortened the duration of arrhythmias during occlusion and reperfusion. Cimetidine 6.9 mg/kg was ineffective to exert the antiarrhythmic action. These results implicate that multiple factors, such as ionic channels (Na, K and Ca), free radicals, arachidonate metabolites and histamine release may play significant roles in genesis of arrhythmias during myocardial ischemia and reperfusion.
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PMID:Drug effects on the ischemia- and reperfusion-induced arrhythmias in the conscious rats. 142 55

Acute coronary occlusion during PTCA represents a significant procedural complication occurring in approximately 4-5% of cases, most frequently because of coronary dissection, spasm, or thrombosis. In these cases the first step in the management of acute ischemia is 1) a brief evaluation of its hemodynamic consequences and 2) the assessment and treatment of its cause. Spasm and intracoronary thrombus formation are usually readily identifiable and treatable using intracoronary nitroglycerin and thrombolytic therapy. In our catheterization laboratory the current approach to occlusive coronary dissection is represented by the use of autoperfusion dilatation catheters and by stent application. The atherectomy devices and the laser "welding" of the dissected intimal segment represent other alternatives that are still under clinical evaluation in this particular setting. If coronary occlusion is refractory to these efforts and coronary blood flow is not reestablished rapidly, emergency coronary bypass surgery is required to salvage jeopardized myocardium. In this case myocardial ischemia may be lessened by the insertion of an intra-aortic balloon pump. In our experience, the incidence of death (4%) and myocardial infarction (37%) for emergency CABG after a failed angioplasty, is similar to that reported by other Authors. The duration of myocardial ischemia and the presence of cardiogenic shock before operation are the most important determinants of major complications such as death and acute myocardial infarction.
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PMID:[Surgical indications and results of myocardial revascularization in complications of PTCA]. 142 76

Spontaneous acute occlusion of the coronary artery produces regional myocardial ischemia and infarction. This coronary occlusion could be due to rapid progression of atherosclerosis or vasospasm. The factors that can precipitate an acute attack of myocardial infarction or coronary spasm are not known. It is proposed that a stress-induced rise of unesterified arachidonic acid could trigger a leukocyte respiratory burst with the release of free radicals such as superoxide anion (O2-), hydrogen peroxide, hydroxyl radical, and singlet oxygen. These free radicals have the ability to inhibit prostacyclin (PGI2) formation and enhance the breakdown of endothelium-derived vascular relaxing factor (EDRF) which are potent vasodilators and platelet anti-aggregators. This may lead to rapid progression of atherosclerosis or coronary vasospasm leading to acute myocardial infarction. If this is true, free radical quenchers and inhibitors of leukocyte oxidative burst may be useful in the prevention of progression of atherosclerosis and coronary vasospasm.
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PMID:Can free radicals induce coronary vasospasm and acute myocardial infarction? 143

To test the hypothesis that the endothelium-derived relaxing factor (EDRF) contributes to coronary vasodilation induced by myocardial ischemia, we examined the effect of NG-nitro-L-arginine (a potent and selective inhibitor of EDRF release) on the coronary reactive hyperemic response in the open-chest dogs. Intracoronary infusion of NG-nitro-L-arginine at a coronary plasma concentration of 5 x 10(-5) M had no effect on hemodynamics and myocardial oxygen metabolism, but attenuated repayment of the flow debt by an average of 20.4% and 20.0% following coronary occlusion for 10 sec and 20 sec, respectively. Concomitant infusion of NG-nitro-L-arginine at the same concentration and 8-phenyltheophylline (a potent adenosine receptor blocker) at a coronary plasma concentration of 10(-5) M further attenuated flow debt repayment following 10 sec and 20 sec of coronary occlusion by 47.7 and 59.4%, respectively. These results indicate that EDRF plays a significant role in the coronary reactive hyperemic response and may cause vasodilation independently of adenosine-mediated vasodilation following coronary occlusion.
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PMID:NG-nitro-L-arginine attenuates flow debt repayment in the reactive hyperemic response of the open-chest dog coronary artery: contribution of endothelium-derived relaxing factor. 144 55


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