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目的观察缺血预适应诱导失血性休克血管反应性和钙敏感性保护。方法采用112只清洁级Wistar大鼠,雌雄各半,体质量220～230g,观察不同失血量(2.5%、5%、10%血容量)、在休克前不同时间(0.5、1、2、3h)缺血预适应,对休克血管反应性和钙敏感性的保护、蛋白激酶Cα(protein kinase Cα,PKCα)和蛋白激酶Cε(protein kinase Cε,PKCε)抑制剂对其保护效应的影响、缺血预适应肠系膜上动脉(superior mesenteric artery,SMA)中PKCα、PKCε的转位。结果①5%血容量休克前0.5h缺血预处理可减轻休克后降低的去甲肾上腺素(norepinephrine,NE)升压效应和收缩血管效应、SMA血管反应性和钙敏感性,使其分别增高25.5%、25.0%、42.3%和40.9%(P<0.01);②PKCα和PKCε拮抗剂可消除缺血预适应诱导的血管反应性保护(分别降低45.0%和72.4%,P<0.01)和钙敏感性保护(分别降低59.0%和52.5%,P<0.01);缺血预适应可促进PKCα和PKCε的转位(P<0.01)。结论缺血预适应通过活化PKCα和PKCε诱导失血性休克后血管反应性和钙敏感性的保护。
Objective To observe the ischemic preconditioning induced hemorrhagic shock vascular reactivity and calcium sensitivity protection. Methods One hundred and twelve clean-grade Wistar rats were randomly divided into male and female rats. The body weight was 220-230g. Different blood loss (2.5%, 5%, 10% ), Ischemic preconditioning, protection against vascular reactivity and calcium sensitivity in shock, the protective effect of protein kinase Cα (PKCα) and protein kinase Cε (PKCε) inhibitors on ischemic Preconditioning of superior mesenteric artery (superior mesenteric artery, SMA) PKCα, PKCε translocation. Results ① 0.5h preconditioning hypoxic ischemic preconditioning can reduce the norepinephrine (NE) vasopressors and vasoconstrictive effects, SMA vasoreactivity and calcium sensitivity after shock, and increase them by 25.5 PKCα and PKCε antagonists could eliminate the protective effect of ischemic preconditioning on vasoreactivity (45.0% and 72.4%, P <0.01, respectively) and calcium sensitivity (59.0% and 52.5%, respectively, P <0.01). Ischemic preconditioning promoted the translocation of PKCα and PKCε (P <0.01). Conclusion Ischemic preconditioning protects vascular reactivity and calcium sensitivity after hemorrhagic shock by activating PKCα and PKCε.