失血性休克引起大鼠肠系膜动脉平滑肌依钙K^+通道活动改变

Hemorrhagic shock induces changes in large-conductance Ca^( 2+)-dependent K^+ channel activity in mesenteric arterial smooth muscle cells of rats

在由股动脉放血制备的失血性休克大鼠模型急性分离的肠系膜动脉平滑肌细胞上 ,利用膜片箝单通道记录技术观察了血管平滑肌依钙K+通道 (BKCa)的活动。发现在对去甲肾上腺素 (NE)反应性增高的休克代偿期 ,BKCa的开放概率 (Po)和单位电导都显著较正常动物的低 ,Po 的改变主要是由通道的慢关闭时间常数 (τcs)增大引起关闭时间延长所致 ;而处于对NE反应性降低的休克失代偿期 ,BKCa的Po 和单位电导都高于正常动物 ,Po的变化也主要是τcs减小所致。

The purpose of the present study was to detect changes in the activity of large conductance Ca 2+ activated K + channel (BK Ca ) during hemorrhagic shock (HS) in mesenteric arterial vascular smooth muscle cells using inside out patches. The HS rat model was produced with withdrawing blood from the femoral artery. The results showed that the BK Ca activity was inhibited with decreased open probability ( P o) and single channel conductance The decrease of P o resulted from an increase of the close time constant (τ cs ) in the compensatory stage of HS, i e the term of hyperresponse of the muscle to norepinephrine (NE) (HS lasted for about 40 min). During the decompensation stage of HS, i e the period of hyporesponse to NE (HS developed for 3 h), the BK Ca activity was enhanced with the increase in single channel conductance and P o which was a result of a decrease in τ cs .