失血性休克后大鼠血管平滑肌舒/缩功能变化及其机制

ALTERATIONS OF CONTRACTILE FUNCTION OF VSM AND IT′S MECHANISM IN HEMORRHAGIC SHOCK RATS

研究失血性休克后大鼠胸主动脉血管平滑肌 (VSM)舒/缩功能变化并初步探讨其发生机制。采用生物张力换能器及生理记录仪等技术体外测定失血性休克后 2、4h大鼠VSM环对去甲肾上腺素 (NE)、苯肾上腺素 (PE)、咖啡因及钾 (K+ )等刺激的收缩反应张力。结果显示 ,VSM环在休克后 2、4h对NE的最大反应张力分别为对照的 76 17%和 6 6 5 0 % ;休克 2h后对 2 0mmol/L咖啡因和高浓度 (>2 0mmol/L)K+ 的反应张力明显下降 ;休克后 4h对 3×10 -6mol/LPE的反应张力亦显著下降。实验结果提示 ,失血性休克后VSM的收缩反应下降 ,其机制可能与休克后VSM细胞胞外钙内流及胞内钙释放能力下降有关。

To investigate the alterations of contractile function of VSM and it's primary mechanism in hemorrhagic shock rats, contractile tension of vascular rings induced seperately by NE,PE,Caffeine and K + was measured with tension conductor and physiological recorder. The results showed that after 2h and 4h of shock, contractile tension of vascular rings to NE was 76 17% and 66 50% as compared to the control group; contractile tension to 20 mmol/L caffeine and over 20 mmol/L K + was significantly decreased after 2h of shock;and decreased to 3×10 -6 M PE after 4h of shock. The data suggested that contractile tension of VSM would decrease after shock and it maybe at least in part related to the decreased function of both calcium influx from ex cells and calcium release from sarcoplasmic reticulum of vascular smooth muscle cells.