Endothelial Dysfunction
Endothelial dysfunction is a risk factor for cerebrovascular events.[30,31]Statin therapy has been shown to improve endothelial function,[25,32,33,34]and there is evidence suggesting that statin therapy is accompanied by increased nitric oxide (NO) bioavailability.[5,35,36] NO modulates endothelial function, affecting both vascular tone and maintenance of a thromboresistant interface between the bloodstream and the vessel wall.[36]
LOW INTENSITY RESISTANCE TRAINING CAN DO THIS
Improvement in endothelial function may, then, be a contributing mechanism to the decreased incidence of stroke observed in patients on statins. For example, studies in a murine experimental model of ischemic stroke show that prophylactic statin therapy enhances cerebral blood flow, reduces infarct size (by approximately 30%), and improves neurologic outcome in normocholesterolemic animals.[37] In this animal model, statin therapy directly upregulated brain endothelial type III NO synthase activity without altering expression of neuronal NO synthase. This effect was independent of change in cholesterol level and was reversible by cotreatment with mevalonate or geranylgeranylpyrophosphate. These observations highlight important cholesterol-independent actions of statins and underscore the potential biologic relevance of intermediates in the cholesterol biosynthetic pathway. In a similar study, atorvastatin has been shown to reduce stroke size in normocholesterolemic mice through cholesterol-independent mechanisms.[38]
LOW INTENSITY RESISTANCE TRAINING CAN DO THIS
Improvement in endothelial function may, then, be a contributing mechanism to the decreased incidence of stroke observed in patients on statins. For example, studies in a murine experimental model of ischemic stroke show that prophylactic statin therapy enhances cerebral blood flow, reduces infarct size (by approximately 30%), and improves neurologic outcome in normocholesterolemic animals.[37] In this animal model, statin therapy directly upregulated brain endothelial type III NO synthase activity without altering expression of neuronal NO synthase. This effect was independent of change in cholesterol level and was reversible by cotreatment with mevalonate or geranylgeranylpyrophosphate. These observations highlight important cholesterol-independent actions of statins and underscore the potential biologic relevance of intermediates in the cholesterol biosynthetic pathway. In a similar study, atorvastatin has been shown to reduce stroke size in normocholesterolemic mice through cholesterol-independent mechanisms.[38]
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