Bravo G, Rojas-Martínez R, Larios F, Hong E, Castañeda-Hernández G, Rojas G, Guízar-Sahagún G
Depto. Farmacobiología, CINVESTAV, IPN, México DF, México.
Life Sci. 2001 Feb 16;68(13):1527-34. doi: 10.1016/s0024-3205(01)00952-3.
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.
在麻醉大鼠中评估了由T5-T6挫伤 procedure 产生的急性脊髓损伤（SCI）所导致的早期心血管效应。在损伤后一小时内测量平均动脉压（MAP）和心率（HR）。损伤后立即观察到MAP和HR显著下降，随后MAP急剧上升。这些变化在3至9分钟之间观察到，20分钟后恢复到基础值。阿托品消除了SCI诱导的MAP和HR下降以及MAP升高。迷走神经切断术中断副交感神经流出也显著减少了MAP的下降和升高以及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）预处理完全消除了SCI产生的效应。这些数据表明，SCI后MAP和HR的下降可能是由于副交感神经纤维释放乙酰胆碱以及内皮来源的NO可能通过胆碱能刺激所致。此外，观察到的MAP升高可能是由于反射性代偿性血管收缩。
