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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male and female, arteriosclerotic and non-arteriosclerotic rats were treated with the anti-lipemic agent, clofibrate, for 8 days and then subjected to an acute myocardial infarction by injecting them with two large doses of isoproterenol spaced 24 hours apart. The animals were killed at sequential time intervals during the acute necrosis and early repair phases of myocardial infarction. Pre-treatment with clofibrate caused a definite improvement in survival, less shock and prostration, and ECG evidence of little or no ischemia. Increased SGOT levels, hepatic lipid and necrosis were indicative of advanced liver damage. Although clofibrate-treated animals showed little change in serum lipids during the acute cardiac necrosis phase, they were hyperglycemic and showed the greatest increase in BUN levels. Clofibrate-treated animals had higher serum corticosterone levels than those given isoproterenol alone. Despite superior survival rates, both the arteriosclerotic and non-arteriosclerotic, clofibrate-treated animals exhibited equally severe histopathologic evidence of myocardial damage. It is suggested that the protective effect of prophylactic treatment with clofibrate against isoproterenol-induced myocardial infarction in rats may be due to its ability to change corticosterone levels in the circulation.
Atherosclerosis 1978 Mar
PMID:Protective effects of clofibrate on isoproterenol-induced myocardial infarction in arteriosclerotic and non-arteriosclerotic rats. 66 86

Acute arterial occlusion in an extremity must be treated as a medical-surgical emergency since not only the affected limb is endangered, but the life of the patient as well. The cause of the acute occlusion is an embolism or in situ thrombosis. The most common source of embolism is the heart from which about 30% of the cardiac emboli obliterate the bifurcation of the femoral artery and about 4/5 of all emboli involve the extremities. Arterio-arterial emboli arise from aneurysms or from nonocclusive, ulcerated atheromatous plaques. Acute in situ thrombosis occurs mostly at the site of stenotic arteriosclerotic lesions. Aneurysms and dilated forms of atherosclerosis can be both the cause of in situ thrombosis as well as the source of an embolism. Differentiation between thrombosis and embolism can be extremely difficult but for acute treatment, however, it is of little relevance. There is a peak of both events in the seventh and eighth decades. On complete occlusion without adequate collaterals, the presentation is characterized by "the six Ps": pain, pallor, pulselessness, paresthesia, paralysis and prostration. With acute occlusion of central points such as the aortic bifurcation or the femoral artery bifurcation, there is complete ischemia with onset of rhabdomyolysis after four to six hours which can lead to severe local and generalized symptoms due to the dangerous metabolites released. In contrast, occlusion of isolated lower leg arteries usually only lead to transient symptoms. If arterial occlusion is suspected, prior to transportation to the hospital, 5000 I.E. heparin should be given intravenously. Acute thrombotic occlusion of large arteries is the surgical domain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of acute peripheral arterial occlusion]. 183 82