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Rescue of Hypoxia/Reoxygenation Induced Impaired Dilation in Rat Cerebral Arterioles

机译:缺氧/雷诺化诱导大鼠脑动脉瘤的扩张受损

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Cerebral arterioles were isolated, cannulated and their vasomotor responses to adenosine tri-phosphate (ATP) observed before and/or after hypoxia (PO_2< 5 mmHg) with rapid normoxic reoxygenation (H/RO). Reoxygenation resulted in a lasting vasoconstriction. Dilation to ATP was significantly decreased. Oxygen radial scavenger or calcium sensitive potassium channel openers restored dilation to ATP but not inhibition of nitric oxide synthase. H/RO directly impaired cerebral arteriolar regulation causing prolonged constriction and reduced dilation which could contribute to the hypoperfusion observed after ischemia/reperfusion and promote neuronal damage, possibly via production of reactive oxygen species (ROS) and subsequent inhibition of calcium activated potassium channels. ROS scavenging or potassium channel openers rescued the vessel response.
机译:分离脑动脉杆菌,腔内和它们的血管振动剂对缺氧(PO_2 <5mmHg)之前和/或缺氧(PO_2 <5mmHg)与快速常规氧化释放(H / RO)观察到的腺苷三磷酸酯(ATP)。 Reoxyenation导致了持久的血管收缩。向ATP扩张显着降低。氧气径向清除剂或钙敏感的钾通道开启器恢复到ATP的扩张,但不抑制一氧化氮合酶。 H / RO直接受损的脑动脉轴调节导致延长的收缩和降低的扩张,这可能导致缺血/再灌注后观察到的低血量熔,可能通过产生反应性氧物质(ROS)和随后的钙活化钾通道的抑制来促进神经元损伤。 ROS清除或钾通道开启者救出了船舶的反应。

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