预处理对失血性休克大鼠肠系膜上动脉收缩反应性的影响

目的评价不同条件预处理对失血性休克血管功能的保护作用机制。方法采用大鼠失血性休克模型，观察不同条件预处理（失血预处理及吡哪地尔预处理）对由激动剂[去甲肾上腺素（NE）]诱导在体大鼠肠系膜上动脉（SMA）收缩反应性的影响。结果5％～10％失血预处理对休克大鼠存活率无显著改善，而吡哪地尔可明显改善休克后120min的大鼠存活率。5％失血预处理30min可上调大鼠休克后0min使用NE前后的股动脉压变化，而预处理24h可降低大鼠休克前股动脉压变化，但对休克后使用NE前后的股动脉压变化无明显影响；吡哪地尔预处理1h可降低大鼠休克前使用NE前后的股动脉压变化，而预处理24h对大鼠休克后的股动脉压变化均无影响。5％失血预处理24h可改善休克后120min大鼠SMA对NE的收缩反应性，使用NE后的管径变化显著增加（P〈0．01）；吡哪地尔预处理1h和24h可明显降低大鼠休克前SMA对NE的收缩反应性，使用NE后的管径变化显著降低（P均〈0．05），但吡哪地尔预处理（1h和24h）均可改善休克后120min大鼠SMA对NE的收缩反应性，使用NE后的管径变化显著增加（P均〈0．05）；而格列苯脲可部分取消吡哪地尔的这一作用。结论吡哪地尔预处理24h可降低休克前大鼠SMA对NE的收缩反应性，并可改善休克后120min大鼠SMA对NE的收缩反应性，且使休克大鼠存活率明显提高。吡哪地尔预处理24h对失血性休克大鼠血管功能的保护作用可能与ATP敏感性钾通道有关。

Effects of preconditioning on the responsiveness of superior mesenteric artery after hemorrhagic shock in rats

OBJECTIVE: To probe the protective effect and mechanism of different ways of preconditioning on vascular function of rats with hemorrhagic shock. METHODS: The hemorrhagic shock model [40 mm Hg (1 mm Hg=0.133 kPa), 120 minutes] was reproduced in rat. The effect of preconditioning (ischemic or pharmacologic) on hyporesponsiveness of superior mesenteric artery (SMA) to noradrenaline (NE) induced by hemorrhagic shock was observed. RESULTS: A loss of 5%-10% blood for preconditioning could not improve the survival rate of rat after hemorrhagic shock, while pinacidial preconditioning significantly increased the survival rate of rats with hemorrhagic shock lasting for 120 minutes. Preconditioning with 5% blood loss for 30 minutes increased the change in femoral artery blood pressure (BP) in rat at 0 minute after shock by the use of NE on mesenteric artery, while the same preconditioning for 24 hours could lower femoral artery BP previous to shock. Pinacidial preconditioning for 1 hour increased the changes in BP before hemorrhagic shock, while pinacidial preconditioning for 24 hours had no significant influence on the change in BP before and after shock. A loss of 5% of blood volume preconditioning for 24 hours improved the vascular responsiveness 120 minutes after hemorrhagic shock, and the change in diameter of SMA was increased significantly before and after the usage of NE (P<0.01). Although pinacidial preconditioning for 1 and 24 hours decreased the responsiveness of SMA to NE before hemorrhagic shock, the changes in diameter of SMA before and after the usage of NE decreased significantly (both P<0.05, respectively), and pinacidial preconditioning (1 and 24 hours) could increase the responsiveness of SMA to NE 120 minutes after hemorrhagic shock, with significantly increased changes of diameter of SMA before and after the usage of NE (both P<0.05). Glybenclamide could partly abolish the effects of pinacidial. CONCLUSION: Although pinacidial (24 hours) could decrease the responsiveness of SMA to NE before hemorrhagic shock, it improves the vascular responsiveness of SMA to NE 120 minutes after hemorrhagic shock, and it improves the survival rate of hemorrhagic shock in rats, suggesting that pinacidial preconditioning (24 hours) could preserve the vascular function after hemorrhagic shock, and ATP sensitive potassium channel may be involved in the process.