Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35