The functional and structural changes in the basilar artery due to overpressure blast injury

摘要: Overpressure blast-wave induced brain injury (OBI) leads to progressive pathophysiologic changes resulting in a reduction blood flow, barrier breakdown, edema, and cerebral ischemia. The aim of this study was evaluate vascular function after single repeated OBI. Male Sprague-Dawley rats were divided into three groups: Control (Naive), OBI (30 psi peak pressure, 1 2 msec duration), (days 1, 4, 7) (r-OBI). Rats killed 24 hours the basilar artery isolated, cannulated, pressurized (90 cm H2O). Vascular responses potassium chloride (KCl) (30 100 mmol/L), endothelin-1 (10−12 10−7 mol/L), acetylcholine (ACh) (10−10 10−4 mol/L) diethylamine-NONO-ate (DEA-NONO-ate) evaluated. resulted an increase contractile endothelin decrease relaxant ACh both r-OBI groups. However, impaired DEA-NONO-ate-induced vasodilation increased wall thickness lumen ratio observed only group. type A (ETA) receptor endothelial nitric oxide synthase (eNOS) immunoreactivity significantly enhanced by These findings indicate that impairs endothelium-dependent dilation, potentially consequence dysfunction and/or remodelling arteries