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

Ten male anginal patients with angiographically documented coronary artery disease, in a randomized double-blind crossover study, smoked one marijuana cigarette (containing 18 mg of delta-9-THC) on one morning and one placebo marijuana cigarette (containing 0.05 mg of delta-9-THC) on a successive morning. Significant increases occurred in average cognitive and intellectual impairment scores, derived from the objective content analysis of 5 min of speech, 30 mins after smoking the marijuana cigarette as compared to the placebo marijuana cigarette, and these scores decreased to near presmoking levels 60 min after smoking. No significant average changes occurred in anxiety or three hostility scale scores following smoking marijuana. Sizable individual differences were noted in the psychological responses to marijuana smoking due, presumably, to personality differences and/or differences in THC pharmacokinetics. Significant psychocardiovascular hemodynamic correlations, as measured by echocardiography, were observed during placebo-marijuana smoking between hostility inward scores and systolic blood pressure and ejection fraction, overt hostility outward scores and diastolic blood pressure, as well as between anxiety scores and stroke volume and left ventricular end-diastolic dimension and left ventricular diastolic volume. These significant psychophysiologic correlations were all eliminated during marijuana smoking. In view of associated findings that marijuana smoking decreased myocardial oxygen delivery, decreased exercise time until the onset of anginal pain, and increased myocardial oxygen demand in anginal patients, the use of marijuana by such patients is clearly inadvisable.
 ...
PMID:Effect of marijuana and placebo-marijuana smoking on psychological state and on psychophysiological cardiovascular functioning in anginal patients. 87 96

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.
 ...
PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35