中文摘要：

目的观察蛋白激酶Cε（PKCε）对失血性休克血管反应性和钙敏感性的调节作用。方法取失血性休克大鼠肠系膜上动脉，利用逆转录-聚合酶链反应（RT-PCR）测定休克即时、0．5、1、2和4h PKCε mRNA的表达；取大鼠肠系膜上动脉一级分支，利用离体血管张力测定技术，测定不同休克时间点的血管环反应性和钙敏感性，并观察PKCε的激动剂和抑制剂对休克2h血管反应性和钙敏感性的影响。结果①大鼠血管反应性和钙敏感性在休克早期增高，晚期进行性降低；正常组织PKCε mRNA表达量低，失血性休克后表达逐渐增加，于1h达到峰值（P〈0.01），4h时仍维持在较高水平（P〈0．01）。②PKCε的激动剂可增高休克2h的血管反应性和钙敏感性，PKCε的抑制剂可降低休克2h的血管反应性和钙敏感性（P均〈0.01）。结论PKCε对失血性休克血管反应性和钙敏感性有重要的调节作用，可能是一种重要的内源性保护分子。

英文摘要：

Objective To observe the regulatory effect of protein kinase Cε（PKCε） on vascular reactivity and calcium sensitivity following hemorrhagic shock. Methods The superior mesenteric artery （SMA） obtained from rats in hemorrhagic shock for different time duration （immediately, 0.5 hour, 1 hour, 2 hours and 4 hours after shock） were adopted to determine the mRNA expression of PKCε using reverse transcription-polymerase chain reaction （RT-PCR） technique, and the first branch of SMA were adopted to assay the vascular reactivity and calcium sensitivity by observing the contraction initiated by norepinephrine （NE） and Ca^2＋ with isolated organ perfusion system. The agonist and antagonist of PKCε were used to observe the regulation of PKCε on vascular reactivity and calcium sensitivity at 2 hours after hemorrhagic shock. Results①Vascular reactivity and calcium sensitivity of the first branch of SMA were increased at the early stage of hemorrhagic shock, and decreased at the late stage of hemorrhagic shock. PKCε mRNA exhibited a time-dependent increase following hemorrhagic shock, peaked at 1 hour （P 〈0.01） and maintained at a high level at 4 hours （P〈0.01）. ②The agonist of PKCε increased the vascular reactivity and calcium sensitivity of the first branch of SMA, and its antagonist decreased the vascular reactivity and calcium sensitivity of SMA at 2 hours after shock （all P 〈0.01）. Conclusion PKCε may be an important endogenous protective molecule. It plays an important role in the regulation of vascular reactivity and calcium sensitization following hemorrhagic shock.