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Mechanisms involved in the cardiovascular alterations immediately after spinal cord injury.

机译:脊髓损伤后立即参与心血管改变的机制。

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The early cardiovascular effects resulting from an acute spinal cord injury (SCI) produced by a contusion procedure at T5-T6 were evaluated in anaesthetized rats. The mean arterial pressure (MAP) and heart rate (HR) were measured during one hour after the injury. A marked decrease in MAP and HR was observed immediately after injury, followed by an abrupt increase in MAP. These changes were observed between 3 and 9 min and the basal values were recovered after 20 min. Fall in the MAP and HR and increase in MAP induced by SCI were abolished by atropine. The interruption of the parasympathetic outflow by vagotomy also significantly diminished the fall and increase in MAP and the fall in HR. Likewise, pre-treatment with nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) completely abolished the effects produced by SCI. These data suggest that after SCI the decrement in MAP and HR was probably due to acetylcholine release from parasympathetic fibers and NO from endothelial source probably by a cholinergic stimulation. Additionally, the MAP increase observed was probably due to a reflex compensatory vasoconstriction.
机译:在麻醉的大鼠中评估了由挫伤程序在T5-T6产生的急性脊髓损伤(SCI)引起的早期心血管效应。受伤后一小时内测量平均动脉压(MAP)和心率(HR)。受伤后立即观察到MAP和HR明显降低,随后MAP突然升高。在3至9分钟之间观察到这些变化,并且在20分钟后恢复了基础值。阿托品消除了由SCI引起的MAP和HR下降以及MAP升高。迷走神经切断术阻断副交感神经外流也显着减少了MAP的下降和增加以及HR的下降。同样,用一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸甲酯(L-NAME)进行的预处理完全消除了SCI产生的影响。这些数据表明,SCI后MAP和HR降低可能是由于副交感神经纤维释放了乙酰胆碱,而内皮源的NO可能是由于胆碱能刺激引起的。此外,观察到的MAP升高可能是由于反射性代偿性血管收缩所致。

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