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目的探讨Rac在失血性休克大鼠血管反应性调节中的作用。方法采用SD大鼠复制休克模型,取离体血管环,观察休克早期和晚期血管反应性的变化以及Rac激动剂和特异性抑制剂对休克早期和晚期血管反应性的影响;通过酶消化法培养原代血管平滑肌细胞(vascular smoot hmuscle cell,VSMC),采用双室培养方式分别观察VSMC缺氧10min和90min后VSMC对去甲肾上腺素(norepinephrine,NE)的收缩反应性变化,同时观察Rac活性调节剂对缺氧后VSMC收缩反应性的影响。结果在休克早期和短暂缺氧后,离体血管环和VSMC对NE收缩反应性均有所升高,Rac的激动剂血小板衍生生长因子(platelet derived growth factor,PDGF)可部分降低休克早期或短暂缺氧后血管反应性,Rac特异性抑制剂NSC23766可拮抗由PDGF所引起的血管反应性的变化,而在休克晚期或长时间缺氧后,离体血管环和VSMC对NE收缩反应性明显降低,NSC23766对休克晚期或长时间缺氧所致血管反应性降低有升高作用。结论休克后血管反应性呈双相变化,休克早期升高,休克晚期降低,Rac参与了休克血管反应性的调节。
Objective To investigate the role of Rac in vascular reactivity regulation in hemorrhagic shock rats. Methods SD rat model of shock was used, isolated vascular rings were taken to observe the changes of early and late vascular reactivity and the effects of Rac agonists and specific inhibitors on early and late vascular reactivity in shock. Cultured by enzymatic digestion Primary vascular smooth muscle cells (VSMCs) were cultured in vitro. The contractile responses of VSMCs to norepinephrine (NE) were observed after hypoxia 10 and 90 minutes, respectively. Meanwhile, the effects of Rac activity Effect of agents on VSMC contractile response after hypoxia. Results In early and transient hypoxia shock, the contractile responses of NE and isolated vascular rings and VSMCs were increased. Rac agonist platelet derived growth factor (PDGF) could partly reduce the early or short-term shock After hypoxia, the vascular reactivity, Rac-specific inhibitor NSC23766, antagonized the changes of vascular reactivity induced by PDGF. However, the contractile responses of isolated vascular rings and VSMCs to NE contractions were significantly lower after shock or prolonged hypoxia , NSC23766 increased the vascular reactivity induced by hypoxia late or long-term shock. Conclusions After reperfusion, the vascular reactivity changes in biphasic phase, the shock increases in the early stage and the shock decreases in the late stage. Rac is involved in the regulation of the vascular reactivity in shock.