Simvastatin Attenuates Experimental Cerebral Vasospasm and Ameliorates Serum Markers of Neuronal and Endothelial Injury in Patients After Subarachnoid Hemorrhage: A Dose-Response Effect Dependent on Endothelial Nitric Oxide Synthase
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چکیده
Delayed cerebral ischemic injury secondary to vasospasm is a major cause of morbidity and mortality after subarachnoid hemorrhage (SAH) (28). Currently, there are no medical treatments that consistently prevent or reverse cerebral vasospasm. Recent studies suggest vasospasm is the result of a multifactorial process leading to a functional imbalance in the cerebrovascular smooth muscle tone (9, 10). Two potential etiologies include microvascular inflammatory cell infiltration and endothelial cell damage, both contributing to a subsequent deficiency of nitric oxide (NO) (6, 7).
منابع مشابه
CORRELATION BE TWEEN ENDOTHELIAL INJURY AND CEREBRAL VASOSPASM FOLLOWING A DOUBLE SUBARACHNOID HEMORRHAGE IN THE RAT
While a wide array of pathological changes occur in cerebral arteries following subarachnoid hemorrhage (SAH), the most consistent is endothelial damage. Since the endothelium normally modulates reflexes that influence vascular tone, any damage to it may represent a significant contributor to cerebral vasospasm following SAH. This experimental study investigates the correlation between end...
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Delayed cerebral vasospasm is an important pathological feature of subarachnoid hemorrhage (SAH). The cause of vasospasm is multifactorial. Impairs nitric oxide availability and endothelial nitric oxide synthase (eNOS) dysfunction has been reported to underlie vasospasm. Memantine, a low-affinity uncompetitive N-methyl-d-aspartate (NMDA) blocker has been proven to reduce early brain injury afte...
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BACKGROUND AND PURPOSE Endothelial nitric oxide synthase (eNOS) activity is decreased after subarachnoid hemorrhage (SAH). Simvastatin increases eNOS activity. We hypothesized that simvastatin would increase eNOS protein and ameliorate SAH-induced cerebral vasospasm. METHODS Mice were treated with subcutaneous simvastatin or vehicle for 14 days and then subjected to endovascular perforation o...
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Reduced endothelial nitric oxide synthase (eNOS) function has been linked to secondary complications of subarachnoid hemorrhage (SAH). We previously found that there is increased eNOS function after SAH but that it is uncoupled, leading to secondary complications such as vasospasm, microthromboembolism and neuronal apoptosis. Here we test the hypothesis that recoupling eNOS with simvastatin can...
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