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)

Clinical, coronary angiographic, and myocardial metabolic data were analyzed to test alternative hypotheses for the pathophysiologic basis of acute coronary insufficiency. The initial incidence of coronary collaterals was not low in relation to coexisting coronary obstructive disease; the early subsequent coronary occlusion rate was high; and in asymptomatic intervals during the acute illness, myocardial hypoxia was infrequent and coronary reserve substantial. These observations support the hypothesis that the acute coronary insufficiency syndrome is caused by reversible coronary ischemic episodes rather than by a new permanent atherosclerotic lesion.
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PMID:The pathophysiologic basis of acute coronary insufficiency. Observations favoring the hypothesis of intermittent reversible coronary obstruction. 91 Jun 78

Previous studies have demonstrated that the positron-emitting fluorine-18 (18F)-labeled fluoromisonidazole is a specific tracer of myocardial hypoxia. Its fractional extraction is enhanced in ischemic or hypoxic myocardium but returns to baseline levels on reperfusion and recovery of normal function. Thus, this agent might be useful in delineating acutely hypoxic but potentially salvageable myocardium. Accordingly, to delineate the relation between the myocardial extraction of 18F-fluoromisonidazole after intravenous administration and the time of antecedent ischemia in vivo, uptake of tracer was measured with positron emission tomography and direct postmortem tissue analysis in 14 dogs in which tracer was administered within 3 h of coronary occlusion (a time associated with marked potential for salvage on reperfusion); in 4 dogs after 6 h of coronary occlusion (a time associated with minimal salvage of myocardium on reperfusion); and in 8 dogs after greater than 24 h of coronary occlusion (to delineate uptake in tissue that is irreversibly damaged). The residual fraction (that is, the amount of tracer extracted and retained in a region) in ischemic myocardium in the dogs in which 18F-fluoromisonidazole was administered within 3 h after occlusion averaged (+/- standard deviation) 23 +/- 18%, which was higher than the residual fraction in myocardium subjected to ischemia for either 6 or greater than 24 h before tracer administration (12 +/- 7% and 5 +/- 2%, respectively, p less than 0.01 for both). Retention of tracer in remote normal myocardium averaged 2 +/- 1%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo delineation of myocardial hypoxia during coronary occlusion using fluorine-18 fluoromisonidazole and positron emission tomography: a potential approach for identification of jeopardized myocardium. 219 19

1. Coronary vasodilator effects of non-ischaemic hypoxia (perfusion with non-oxygenated Tyrode solution) and ischaemic hypoxia (coronary occlusion) were compared. 2. The left anterior descending coronary artery (LAD) of six in situ canine hearts was perfused selectively at controlled pressure with normal arterial blood or with non-oxygenated Tyrode solution. LAD flow was measured continuously with an electromagnetic flowmeter. Reactive hyperaemic blood flow responses following 3 min Tyrode perfusion were compared with responses following 3 min complete coronary occlusion. 3. Control LAD blood flow was 26.9 +/- 4.6 ml/min. A 3 min period of Tyrode perfusion caused a peak reactive hyperaemic blood flow of 151 +/- 31 ml/min, which was not significantly different from that caused by 3 min occlusion, 123 +/- 17 ml/min. The duration and total volume of reactive hyperaemia flow following Tyrode perfusion were smaller than values following occlusion. 4. The present findings demonstrate that myocardial hypoxia per se is a sufficient vasodilatory stimulus to account for the peak reactive hyperaemic flow following 3 min occlusion, but that the prolonged reactive hyperaemic response depends on vasodilator metabolites which accumulate in ischaemic myocardium.
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PMID:Perfusion with non-oxygenated Tyrode solution causes maximal coronary vasodilation in canine hearts. 344 93

Several studies have suggested that L-carnitine may limit the cellular alterations induced by myocardial hypoxia or ischemia. In the present study, rats were subjected to chronic treatment with L-carnitine (0, 25, 50 or 200 mg/kg/day i.p.) for 9 days prior to being submitted to permanent regional myocardial ischemia by left coronary artery ligation in situ. Following 48 hours of coronary occlusion, infarct size was measured using planimetry of transverse sections of the hearts, which had been stained with nitro-blue tetrazolium. Various functional and metabolic parameters have also been measured in isolated perfused hearts. Treatment with L-carnitine at 200 mg/kg/day i.p. for 9 days led to a significant reduction in infarct size and a better preservation of residual cardiac function. However, none of the metabolic parameters measured were modified. In conclusion, we suggest that the preservation of cardiac contractile function observed with L-carnitine pretreatment is secondary to carnitine-induced infarct size limitation.
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PMID:Cardioprotective effect of L-carnitine in rats submitted to permanent left coronary artery ligation. 751 37

Myocytes in the border zone of myocardial infarction are under severe hypoxia without characteristic morphology of necrosis, and show ultrastructural features similar to those seen within the first hours after coronary occlusion. This study was carried out to evaluate the possibility that immunohistochemical methods could be used for the early diagnosis of myocardial infarction by detecting areas of hypoxia. Nineteen human sections of formalin-fixed paraffin-embedded myocardial samples showing a necrotic area and its border were submitted to immunohistochemical staining with the markers antimuscle actin, antimyoglobin, antitroponin T, antifibronectin, and anticomplement component C9. Sections were also subjected to azan trichrome and hematoxylin-basic fuchsin-picric (HBFP) staining techniques. Immunohistochemistry and azan trichrome showed that in the border zone there was a pattern of reaction intermediate between the infarcted area and the normal myocardium. The HBFP failed to distinguish these two areas. In conclusion, immunohistochemistry and azan trichrome can recognize myocardial hypoxia. Because hypoxia is an invariable condition in infarction, these techniques can be used to confirm suspected cases of myocardial infarction in which necrosis is not yet evident. However, considering that agonal states may be associated with generalized hypoxia, further studies are needed to confirm the reliability of this procedure in the earlier phases of myocardial infarction.
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PMID:Is immunohistochemistry a useful tool in the postmortem recognition of myocardial hypoxia in human tissue with no morphological evidence of necrosis? 1195