Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.
Am J Cardiol 1976 Oct
PMID:Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block. 97 Mar 29

Free nucleotide, polyamine and nucleic acid synthesis was studied in myocardial acute ischemia and reperfusion. An early stimulation of biosynthesis of these compounds was observed during ischemia, than later, a remarkable decrease of their specific radioactivity appeared. Reperfusion experiments cause a significant increase of nucleic acids and related compound biosynthesis. The results indicate that the biochemical mechanism of myocardial protein synthesis, under our experimental conditions are not irreversibly damaged by ischemia. In fact, the reperfusion causes a remarkable recovery of nucleic acid, free nucleotide and polyamine specific radioactivity. The changes during the period of infarction and subsequent reperfusion show that polyamines play a key role in myocardial ischemia and reperfusion.
G Ital Cardiol 1976
PMID:Experimental revascularization of acute myocardial infarction. III: Correlation between the behaviour of the free nucleotide acid solubles and some aliphatic biogenic amines. 97 65

The aim of this study was to investigate the action of isoproterenol (ISP) on the myocardium by means of light microscopy, histochemistry, autoradiography with tritiated ISP and electron microscopy. One hundred and sixty four Wistar rats were divided into 8 groups. Group A, B, C and D were given 10 mg/kg i.p. ISP (plus 5 uC of tritiated ISP). The animals were sacrificed at different intervals. Group E served as control to proceeding groups. Group F was given 10 mg/kg i.p. ISP and subjected to "holding" stress; Group G was its corresponding control. Group H received 9 mg/kg. prenylamine, as inhibiting drug, 1 hour before and hour after ISP injection. Histopathology of "infarct like" lesions presenting localized necrosis, myocytolysis, homogenization and positive tests for ischemia are correlated to the localization of tritiated ISP on sarcolemma and to changes in succine dehydrogenase enzymes in the groups A, B, C and D. Hypercontraction and widening of Z bands of sarcomers are found in electron microscopy. These ischemic changes are inhibited by prenylamine, a drug acting as moderator of catecholamine effects by slowing down Ca transport. It is concluded that myocardial necrosis induced by ISP is probably due to an increased activation of the "calcium pump". The ISP provoked lesions appear to be a promising model to study experimental myocardial necrosis.
Arch Inst Cardiol Mex
PMID:Pathogenesis of isoproterenol-induced lesions in the rat myocardium. 98 94

Studies of the pulmonary circulation in normal man, performed with external radiation detectors, have shown that pulmonary blood volume is about 10% of total blood volume. Pulmonary blood volume was unchanged in patients with acute or chronic left atrial hypertension and in normal persons during expansion of total blood volume in spite of marked increases in pulmonary vascular pressures. However, pulmonary blood volume was greatly increased in patients with polycythemia rubra vera and a large total blood volume and in patients with a left to right shunt but normal pulmonary intravascular pressure. Studies of regional myocardial perfusion with injection of xenon-133 solution into the left coronary artery revealed localized areas of ischemia distal to stenotic lesions even when the patient was at rest. During angina produced by pacing, more severe ischemia occurred, thus suggesting that functional factors reduce local perfusion below resting levels. In patients with "variant" angina, intravenous injection of thallium-201 chloride during spontaneous attacks has revealed large cold areas in myocardial scintigrams not present under control conditions, thus suggesting severe transmural reduction of perfusion in heart muscle corresponding to S-T segment elevation in the electrocardiogram.
Am J Cardiol 1976 Nov 23
PMID:Pathophysiologic studies of the pulmonary and coronary circulations in man. 99 14

Using epicardial electrograms others have established that infusion of isoproterenol increases myocardial injury after acute coronary occlusion. To define the contribution of alterations in collateral blood flow to this increased ischemia, isoproterenol was administered to 10 dogs. After pretreatment with practolol in doses that successfully block inotropic but not vascular effects of beta adrenergic stimulants, intracoronary isoproterenol continued to enhance the magnitude of S-T segment elevation in ischemic areas. Thus, vasodilation induced by isoproterenol appears to divert flow from the ischemic area. To test this hypothesis, intracoronary adenosine was given to cause coronary vasodilation without enhancing inotropy. S-T segment elevation at ischemic and adjacent sites was significantly increased. Neither agent had systemic effects, but each increased coronary blood flow while concomitantly decreasing collateral flow as evidenced by a reduction in retrograde coronary flow and peripheral coronary pressure. In addition, adenosine significantly diminished the rate of xenon-133 clearance from the ischemic myocardium. Thus, isoproterenol, in addition to its positive inotropic effect, increases myocardial injury by its vascular action. Collateral blood flow to acutely ischemic myocardium is diminished by the production of a coronary steal. Intravenously administered isoproterenol additionally diminishes collateral flow by decreasing coronary perfusion pressure. It is postulated that any agent that causes either a primary or secondary coronary vasodilation may cause a coronary steal and subsequently enhance myocardial injury.
Am J Cardiol 1976 Dec
PMID:Coronary steal: its role in detrimental effect of isoproterenol after acute coronary occlusion in dogs. 99 23

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
Am J Cardiol 1976 Dec
PMID:Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases. 99 29

Some of the laboratory difficulties in assessing infarction size produced by intermittent coronary artery occlusion were demonstrated by using an epicardial mapping technique in anesthetized open-chest dogs. Intermittent occlusion of a left anterior descending coronary artery branch resulted in a marked elevation of the ST segment above the baseline in the areas of the myocardium supplied by this vessel. Repeated occlusions after administration of normal saline as a control produced less ST-segment elevation thn that noted during control occlusions; however, repeated occlusions after infusion of quinidine produced a further lessening in ST-segment elevation. The problems encountered in interpreting these results are emphasized. Long-term coronary occlusion studies were performed in order to correlate epicardial electrograms with histological findings of ischemia or myocardial necrosis. Our investigations show that epicardial mapping tended to underestimate the area of injury, and this limits the interpretation of drug intervention studies such as those in which quinidine is administered. Therefore, caution should be exerted when using epicardial mapping techniques to assess the effect of various pharmacological interventions on infarction size in open-chest dogs.
Eur J Cardiol 1976 Dec
PMID:Problems in assessing infarction size by epicardial mapping: preliminary studies with quinidine. 100 38

Our series (30 cases) of variant angina as well as the reports from literature, were reviewed, to investigate the consequences of an acute regional ischemia on seno-atrial, atrio-ventricular and intraventricular conduction. Sinoatrial conduction was never affected independently from the anterior or posterior localization of the ischemia. A junctional impairment of atrio-ventricular conduction was rather frequent in cases of variant angina affecting the inferior wall, ranging in different series from 8% to 25%. Only one case of bundle branch block was observed. Hemiblocks were found to be extremely rare, while a deviation of the main axis of the QRS on the frontal plane, especially to the left in cases with anterior localization of the ischemia, was observed quite frequently. This axis deviation, in the absence of changes of the initial vector of the QRS compatible with the diagnosis of hemiblocks, were considered to be depending on a parietal block.
G Ital Cardiol 1976
PMID:[Prinzmental's angina and disturbances of the stimulus conduction (author's transl)]. 101 Jan 72

The behaviour of some enzymatic activities, such as monoamino oxidase (MAO), diamino oxidase (DAO), catalase, peroxidase and creatin chinase (CPK) have been studied both in blood serum and myocardial tissue of acute infarcted dogs (obtained by coronary occlusion). The most significant results are the changes of the DAO activity (--50% from the control) and peroxidase activity (+60%), 6 hours after acute ischemia. The effect of reperfusion was studied 2 hours later. A recovery of DAO activities was shown, while the peroxidase activities stayed elevated. All the enzymatic activities studied were evaluated in the serum, under the same experimental conditions. An increase of all these activities was observed until 6th hour of coronary occlusion. The reperfusion of acute ischemia, after six hours, causes a further increase of CPK and MAO activities and a decrease of catalase peroxidase and particulary evident DAO activities. The results of this experiment show that reoxygenation, under our experimental conditions, increases a further enzymatic release and in part causes a metabolic recovery of heart muscle.
G Ital Cardiol 1976
PMID:[Experimental revascularization of acute myocardial infarction. II: Activity of various oxidoreductive tissutal and serum enzymes (author's transl)]. 101 Jan 98

In order to study the arterial blood supply of the sinus atrial node in the Dog, the authors have performed the post-mortem injection of the arterial branches going to this node. They observed 65 cases and they came to the following conclusions: in 31 cases (47.7%) the sinus atrial node is supplied by the artery of the sinus atrial node and by the anterior atrial artery, branch of the circumflex; in 20 cases (30.8%) besides the two arteries already mentioned there was also the anterior branch from the first portion of the right coronary artery; in 13 cases (20%) the sinus atrial node was exclusively supplied by the artery of the sinus atrial node and in one case (1.5%) it was supplied only by the first anterior atrial branch of the circumflex artery. Their findings are different from those of other authors and they attribute the failure in provoking experimental ischemia of the sinus atrial node in the Dog, to the rich blood supply of this node and to the different origins of the vessels supplying it.
Acta Cardiol 1975
PMID:[Arterial vascularization of the sino-auricular node of the heart in dogs]. 108


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