Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A considerable number of large scale clinical trials provide clear evidence that cholesterol lowering is one of the most important risk-reduction strategies for secondary and primary prevention of coronary artery disease. Unlike the older studies with fibrates, the most recent trials of cholesterol-lowering therapies with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have clearly shown that their use can reduce coronary artery disease and total mortality as well as the need for expensive hospitalization and revascularization procedures. Studies such as the Scandinavian Simvastatin Survival Study (4S), the West of Scotland Coronary Prevention Study (WOS), the Cholesterol and Recurrent Events (CARE) trial and most recently the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) as well as numerous other investigations, have established that decreasing elevated levels of low-density lipoprotein (LDL) cholesterol will result in a reduction in risk of coronary artery disease. In addition, HMG-CoA reductase inhibition reduces the risk for cerebral ischemia. Recent data indicate that less than half of patients with coronary artery disease receive cholesterol-lowering therapy, and few meet the LDL-cholesterol goal. Therefore clinicians treating coronary artery disease need to emphasize secondary prevention and recognize the key role of cholesterol-lowering therapy. The challenge for clinicians is to apply the important lessons learned from these clinical trials to an "evidence-based" patient care.
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PMID:[Prevention of coronary heart disease--"evidence-based medicine" of antilipemic therapy]. 1009 8

3-hydroxy-3-methyl-glutaryl-coenzyme-A (HMG-CoA) reductase inhibitors (statins) have been shown to protect against ischemic stroke by mechanisms that are independent of lowering serum cholesterol levels. In this study we investigated the potential neuroprotective effect of a single i.v. treatment with four increasing doses of pravastatin on permanent occlusion of middle cerebral artery (MCAo) in spontaneously hypertensive rats. Pravastatin was given 10 min after MCAo and its effect was determined 24 h later. Treatment results were evaluated in terms of infarct volume, homolateral hemisphere oedema, glial fibrillary acid (GFAP), vimentin (Vim) and endothelial NO synthase (eNOS) immunoreactivity and TUNEL positivity. Cerebral levels of eNOS were measured by western blot analysis. Pravastatin did not reduce cerebral infarct while it mitigated homolateral hemisphere oedema in a dose-dependent manner with respect to controls. No differences among groups were found regarding GFAP and Vim immunoreactivity and TUNEL positivity. Instead, pravastatin-treated animals presented a more marked cerebral eNOS immunoreactivity as compared with controls. In agreement with immunohistochemistry, immunoblot revealed dose-dependent increases in cerebral levels of eNOS in pravastatin rats. Our data confirm statin neuroprotection in cerebral ischemia. In particular, it is of great interest that a single i.v. Pravastatin administration reduced cerebral oedema by upregulating eNOS expression/activity. This, by increasing vascular NO bioavailability, could have produced proximal vasodilation and contributed to reducing perfusional deficit. It is worthy stressing how important the anti-oedema action is that pravastatin seems to exert. Indeed, cerebral oedema, when widespread and beyond limits of physiological compensation, causes endocranic hypertension and additional cerebral damage over time.
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PMID:Intravenous administration of pravastatin immediately after middle cerebral artery occlusion reduces cerebral oedema in spontaneously hypertensive rats. 2149 97