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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 investigate the changes of intracellular pH in severe hemorrhagic shock vascular smooth muscle cells and to clarify the relationship between intracellular acidosis and decreased vascular reactivity. Methods Smooth muscle cells of arterioles were isolated by laser confocal microscopy. Fluorescence probe labeled pH value of smooth muscle cells were measured by laser confocal microscopy. Plasma and ATP-sensitive potassium channel (KATP) Acidosis rats were subjected to local and systemic treatment to observe the effects on vascular reactivity. Results Severe hemorrhagic shock vascular reactivity was significantly lower, smooth muscle cells within the acidosis; alkali treatment can improve intracellular acidosis, but only partially restored vascular reactivity; glyburide can improve shock and simple acidosis caused by low blood vessels Reactivity. Conclusion Severe hemorrhagic shock in the smooth muscle cells acidosis, is one of the important causes of hyporesponsiveness. Intracellular acidosis activates KATP channels and is involved in the mediation of hypovascular reactivity.