血管平滑肌细胞内酸中毒在重症休克血管反应性降低中的作用  

The Role of Intracellular Acidosis of Arteriolar Smooth Muscle in the Pathogenesis of Vascular Hyporeactivity During Severe Hemorrhagic Shock

作　　者：刘杰[1] 赵克森[1] 王雪梅[1] 黄绪亮[1] 

机构地区：[1]第一军医大学病理生理学教研室,广州510515

出　　处：《中华创伤杂志》1999年第S1期11-14,共4页Chinese Journal of Trauma

摘　　要：目的　查明重症失血性休克血管平滑肌细胞内pH改变 ,阐明细胞内酸中毒与血管反应性降低间的关系。方法　分离细动脉平滑肌细胞 ;用激光共聚焦显微镜测定荧光探针标记的休克平滑肌细胞内pH值 (pHi) ;以碱性液体及ATP敏感钾通道 (KATP)阻滞剂优降糖对休克及单纯酸中毒大鼠进行局部和全身治疗 ,观察对血管反应性的影响。结果　重症失血性休克时血管反应性明显降低 ,平滑肌细胞内发生酸中毒 ;碱治疗能改善细胞内酸中毒 ,但仅部分恢复血管反应性 ;优降糖能提高休克及单纯酸中毒引起的低血管反应性。结论　重症失血性休克时平滑肌细胞内发生酸中毒 ,是血管反应性低下的重要原因之一。细胞内酸中毒激活KATP 通道 ,参与介导低血管反应性的发生。Objective To study the intracellular pH changes of arteriolar smooth muscle cells and to elucidate the relationship between intracellular acidosis and vascular hyporeactivity in severe hemorrhagic shock (HS). Methods HS model was reproduced. Arteriolar smooth muscle cells were loaded with Snafl calcein-AM to measure intracellular pH with confocal microscopy when arteriolar hyporeactivity to norepinephrine (NE) occurred. The animals were treated with alkaline solution or glibenclamide in situ or systematically, and their effect on vascular hyporeactivity was observed. Results Intracellular acidosis of smooth muscle presented when arteriolar hyporeactivity occurred during HS. Alkaline solution could improve intracellular acidosis, but only increased vasoreactivity partially. Glibenilamide could restore vascular hyporeactivity caused by HS and acidosis in situ. Conclusions Intracellular acidosis of smooth muscle cells is one of the important factors for arteriolar hyporeactivity in HS. Excessive intracellular H + induces activation of K ATP channel and mediates the arteriolar hyporeactivity.

关 键 词：休克 出血性 酸中毒 肌 平滑 血管 H^+-K^+交换ATP酶 

分 类 号：R364[医药卫生—病理学]