摘要
目的：研究血管平滑肌钙动力学变化在重症休克血管反应性降低中的作用．方法：复制大鼠失血性休克模型，测定脊斜肌细动脉对去甲肾上腺素（ＮＥ）反应性；用激光共聚焦显微镜测定单个平滑肌细胞钙动力学变化；观察ＡＴＰ敏感钾通道（ＫＡＴＰ）阻滞剂优降糖对血管反应性和钙动力学影响．结果：大鼠失血休克后１～２小时细动脉对ＮＥ反应性显著下降，ＮＥ升高细胞内钙离子浓度的作用明显减弱，以外钙内流减弱最为明显．优降糖明显提高休克时ＮＥ对平滑肌细胞内钙离子的升高作用，改善细动脉对ＮＥ反应性．结论：重症失血性休克血管反应性低下与ＫＡＴＰ通道开放导致细胞外钙内流减少有关．
Aim: To study the role of calcium kinetic changes in vascular hyporeactivity in severe hemorrhagic shock (HS). Methods: HS model was made and the response of arterioles in spinotrapezius muscles to norepinephrine (NE) in HS was tested. The calcium kinetic changes were measured with confocal microscopy, and the effect of glibenclamide, a specific inhibitor for ATP sensitive potassium (KATP) channel, on vascular reactivity and the concentration of intracellular calcium ions ([Ca2+]i) were studied. Results: HS for 1￣2 hours caused a reduction of vasoreactivity to NE and on the effect of NE making [Ca2+]i rise in arteriolar smooth muscle cells. The reduction of [Ca2+]i rise was largely caused by the decrease of Ca2+ entry from extracellular sources. Glibenclamide could improve NE effect on、 [Ca2+]i as well as vasoreactivity. Conclusion: Vascular hyporeactivity in HS was partly due to the reduction of membrane Ca2+entry which was induced by activation of KATP channel and membrane hyperpolarization. Glybenclamide can increase vasoreactivity, which may be a new way to the treatment of hemorrhagic shock.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
1997年第6期333-335,共3页
Chinese Journal of Trauma
基金
军队九五重点课题
关键词
失血性休克
血管反应性
钙动力学
Hemorrhagic shock Arteriole Vasoreactivity Calcium KATP channel
