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)

In the first few hours after acute coronary thrombosis, clinical coronary angiography is associated with enhanced risk of ventricular fibrillation. In these experiments, the ventricular fibrillation threshold (VFT) was measured in anesthetized dogs before and during acute occlusion of the left circumflex coronary artery. Ischemia alone reduced the fibrillation threshold. Angiography with 1- or 2-ml does of Renografin 76 lowered VFT significantly more than did equal doses of iohexol or iopamidol. It is concluded that nonionic agents may be safer for coronary angiography in the presence of acute coronary insufficiency.
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PMID:Changes in ventricular fibrillation threshold induced by contrast agents during acute coronary artery occlusion. 686 5

This paper is a synopsis on recent reports dealing with the pharmacological basis of molsidomine-induced circulatory effects. The therapy of coronary insufficiency by molsidomine is based on different pathophysiological and pharmacological mechanisms. The inactive compound molsidomine is metabolized--mainly in the liver--to form the vasoactive and antiaggregatory compound SIN-1 and SIN-1A. Due to the gradual conversion into the active compound, the peak effects are observed only after 15 min (intravenously) or 30 to 60 min (orally). The effects are long-lasting and can be observed up to four to six hours. The c-GMP mediated dilation of various vascular sites comprise mainly the venous system (both small and large veins), resulting in a significant preload reduction, a decrease in cardiac output, a decrease in heart size and circumferential wall stress, a decrease in myocardial oxygen consumption and a therapeutically important improvement of O2-delivery versus myocardial O2-consumption. This effect results in a significant improvement of myocardial ischemia (reducing frequency of anginal attacks, improvement of exercise tolerance and of exercise induced ST-depressions). In animal experiments molsidomine diminishes infarct size and suppresses reperfusion-induced ventricular fibrillation following ischemia. Molsidomine dilates, like nitroglycerin, the large coronary arteries. Therefore, in coronary heart disease, it may improve collateral flow in addition to beneficial effects on subendocardial perfusion resulting from the reduction of ventricular wall stress. In addition to direct dilating effects on collateral vessels an improvement in perfusion of asynergistically contracting ventricular sections has been observed. In contrast to nitroglycerin, effects on peripheral resistance appear only under extremely high dosages and reflex increases in heart rate are rarely observed. In general molsidomine-induced changes (increases) in heart rate, in stroke volume (decreases), and in cardiac output (decreases) are of small magnitude. Recently interesting findings on molsidomine-induced suppression of thrombocyte aggregation, of thromboxan-synthesis inhibition and of increased prostacyclin formation have been presented, which may be important in the improvement of myocardial (micro-) circulation under ischemic conditions.
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PMID:[Pharmacological basis of therapy with molsidomine]. 689 44

Prostacyclin, a substance produced by vessel wall, has a sustained vasodilating and platelet antiaggregating activity and therefore the variations in its production in patients with ischemic heart disease are of interest. Prostacyclin production was assessed in 59 patients with ischemic heart disease and 59 control subjects matched for age, sex, body weight, smoking habits, blood pressure and serum cholesterol levels. Of the 59 patients examined, 23 had had a myocardial infarction 3 to 12 months earlier; 21 had had spontaneous angina and 15 effort angina for at least 3 months. Patients with myocardial infarction and spontaneous angina were also classified in subgroups with and without acute coronary insufficiency, according to the occurrence of ischemic attacks in the week preceding the study. Both circulating prostacyclin levels and prostacyclin produced after 3 minutes of ischemia were measured by bioassay. Circulating prostacyclin was significantly less in patients with ischemic heart disease than in matched control subjects independent of the clinical type of ischemic heart disease. Circulating prostacyclin was particularly reduced in patients with acute coronary insufficiency in comparison to patients without, both in the group with myocardial infarction (1.11 +/- 0.22 ng/ml and 2.09 +/- 1.32, respectively) and in the group with spontaneous angina (1.24 +/- 0.42 and 2.17 +/- 1.16, respectively). No differences could be found for prostacyclin produced after 3 minutes of ischemia in relation to the presence of acute coronary insufficiency. The lower level of prostacyclin production in patients with ischemic heart disease and especially in those with acute coronary insufficiency may be an important factor in the occurrence of coronary occlusion or spasm.
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PMID:Reduced prostacyclin production in patients with different manifestations of ischemic heart disease. 703 88

The literature data indicating nonspecific pathologic symptoms of the circulatory system in those occupationally exposed to caprolactam and diphenyl inspired the authors to evaluate the circulatory system in a group of 495 workers of a Chemical Plant producing polyamide fibres. The anamnestic data, family inquiry and subjective changes indicate that any hints of the significant effects of the technological process on circulatory diseases in this professional group are unwarranted. The percentage values of the latent circulatory failure (1-2% of subjects), coronary insufficiency (6.6% of subjects), arterial hypertension (5.7% of subjects) did not show any significant differences, as compared to the control group and normal Polish population. The obtained results of ECG test evaluated according to the Minnesota-Code criterion did not significantly differ from 100 controls composed of those in whom no changes in the circulatory system were found, whereas clear differences were found related to 50 persons with documented heart ischemia.
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PMID:[Evaluation of the circulatory system in workers exposed to caprolactam and diphenyl in 1 of the chemical plants producing polyamine fibers]. 704 58

The data obtained in experiments on 89 random bred male white rats indicate an important pathogenetic role of lipid peroxidation activation during ischemia of the myocardium and its further reperfusion. Inhibition of lipid peroxidation by sodium selenite was accompanied by increased resistance of the heart to its reversible ischemia. The evidence obtained documents a new principle of pathogenetic therapy of transitory coronary insufficiency with lipid peroxidation inhibitors, particularly sodium selenite. The data presented may be of importance for clinical practice since transitory myocardial ischemia in animals represents an experimental model of the forms of coronary heart disease of man which are accompanied by transient reduction of the coronary blood flow.
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PMID:[Pathogenetic role of lipid peroxidation and the protective role of sodium selenite in ischemia and myocardial reperfusion]. 724 94

Experiments on 115 noninbred male rats demonstrated that activation of lipid free-radical peroxidation during transitory coronary insufficiency was observed both in myocardial ischemia and subsequent reperfusion of the heart. The increase in lipid chemiluminescence during the recovery of the coronary blood flow was more pronounced after long-term myocardial ischemia. It was shown that activation of lipid peroxidation during reperfusion was accompanied by the increment of the myocardial content of the peroxidants--adrenaline, oxygen and calcium ions. It is suggested that activation of lipid free-radical peroxidation may be one of the principal factors responsible for the increased myocardial alteration during reversible ischemia, as well as during temporary failure of the coronary blood flow seen in the coronary heart disease of man.
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PMID:[Mechanisms of free radical liquid peroxidation activation during regional ischemia and subsequent reperfusion of the heart]. 729 82

12 patients suffering from chronic coronary insufficiency with signs of ischemia in the ECG, were treated orally with 200 mg of acebutolol t.i.d. for a period of 3 weeks. The following parameters were examined at the beginning of the therapy as well as at the end of every week: number of stenocardiac attacks, characteristics of pain, nitroglycerin consumption, B.P., H.R., respiratory rate, ECG, maximal exercise test, PEP, LVET, PEP/LVET at rest and immediately after effort. The treatment with acebutolol was effective inducing an improvement of subjective symptoms (reduction of stenocardiac crises, intensity and duration of angor, trinitrin pearls consumption) and an increase of effort tolerance. The utility of the therapy was also proved by the reduction of the systolic pressure and by the following decrease of hemodynamic overload and, therefore, of the heart muscle's work. This positive effect is due to the reduction of the myocardial oxygen consumption, modulated among others by the bradycardiac action of the drug. The cardioselectivity of acebutolol avoided to cause peripherical disorders usually observed with other non selective beta blocking drugs.
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PMID:[Effects of the administration of acebutolol in patients with chronic angina of effort]. 730 53

One hundred cases with an admission diagnosis of acute coronary insufficiency or unstable angina were reviewed to establish criteria for admission to a coronary care unit. Myocardial infarction was subsequently diagnosed in 20 of the patients. Ventricular tachycardia occurred in 16 patients and ventricular fibrillation in 1 patient. Clinical features found to predict an increased risk of myocardial infarction included chest pain for more than 30 minutes within 24 hours prior to admission, new nonspecific electrocardiographic abnormalities consistent with ischemia, and diaphoresis. All patients with ventricular tachydysrhythmias had presented with both prolonged chest pain prior to admission and new electrocardiographic changes. The sensitivity, specificity and predictive value of various clinical criteria for identifying patients likely to have a myocardial infarction were calculated, and criteria with very high (greater than 90%) sensitivity were identified. These could be used to establish which patients are at increased risk of myocardial infarction and therefore require admission to a coronary care unit.
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PMID:Indications for admission to a coronary care unit in patients with unstable angina. 736 10

Hearts of 38 men dying suddenly of acute coronary insufficiency and autopsied within 3 hours after death were examined. Foci of acute ischemic injuries in different parts of the myocardium were studied by histochemical methods for which the activity of succinate dehydrogenase and phosphorylase were determined. Early ischemic lesions in the myocardium were found in 22 fatalities, of them 5 had acute myocardial infarction, in 9 foci of ischemia were combined with the presence of postinfarction scars and fine focal cardiosclerosis, in 8 cases foci of early ischemia were the only changes in the myocardium. The majority of the decreased had stenosing atherosclerosis of the coronary arteries. Localization of ischemia foci in the myocardium did not always correspond to the severity of stenosing or the presence of thrombosis of the artery supplying the corresponding parts of the heart muscle. No foci of ischemia in the myocardium were found in 16 decreased who also had quite marked coronary atherosclerosis.
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PMID:[Early ischemic injuries of the myocardium in sudden cardiac death]. 742 69

The cardiac counter-indications to exercise training for a patient with peripheral arteriopathy are seldom absolute: it is the case of evolutive coronary insufficiency or cardiac insufficiency, or serious rhythm disturbances not controlled by treatment. The exercise test on a cycle ergometer can distinguish coronary or either peripheral arterial disease is predominant. If the arteriopathy is dominant, the rehabilitation program may be pursued unhindered, although one must remain vigilant. If the coronary disease is predominant, one must teach the patient not to go above the heart rate at which the ischemia appears on the E.K.G.
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PMID:[The effects of coronary insufficiency on physiotherapy for peripheral arteriopathy (author's transl)]. 746 52


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