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目的观察调控RhoA/Rac平衡在休克后血管反应性双相变化中的作用。方法采用失血性休克模型,分别取RhoA、Rac激动剂或抑制剂,观察其对休克早期或休克晚期大鼠平均动脉血压(mean arterial pressure,MAP)、肠系膜上动脉血管管径对去甲肾上腺素(norepinephrine,NE)收缩反应性的影响。结果失血性休克后整体动物肠系膜上动脉对NE的收缩反应和NE的升压反应呈双相变化,休克早期升高,休克晚期降低。Rac激动剂血小板衍生生长因子(platete-derived growth factor,PDGF)和RhoA特异性抑制剂C3转移酶可降低休克早期肠系膜动脉对NE收缩反应性和NE升压反应性;RhoA激动剂U-46619和Rac特异性抑制剂NSC23766可改善休克晚期肠系膜上动脉对NE的收缩反应和NE的升压效果,也进一步升高休克早期收缩反应性;RhoA激动剂U-46619和Rac激动剂PDGF的作用可以分别被其特异性抑制剂所拮抗。结论用RhoA或Rac激动剂或拮抗剂可调控失血性休克大鼠血管反应性双相变化,提示休克早期RhoA活性升高,Rac活性降低,而休克晚期RhoA活性降低,Rac活性升高,RhoA/Rac活性平衡参与了休克后血管反应性双相变化的调节。
Objective To observe the role of regulation of RhoA / Rac balance in biphasic changes of vascular reactivity after shock. Methods Hemorrhagic shock model was adopted. RhoA and Rac agonists or inhibitors were respectively administered to observe the effects of mean arterial pressure (MAP), vascular diameter of superior mesenteric artery and norepinephrine (norepinephrine, NE) contractile reactivity. Results After hemorrhagic shock, the contractile responses of the superior mesenteric artery to NE and NE increased in response to biphasic changes. The shock increased in the early stage and decreased in the late stage of shock. Rac agonist platelet-derived growth factor (PDGF) and RhoA-specific inhibitor C3 transferase could reduce NE contractile response and NE hyperresponsiveness in early mesenteric artery of shock. RhoA agonist U-46619 and RacA inhibitor U-46619 and Rac agonist PDGF could enhance the contractile response of NE and the effect of NE in shocked superior mesenteric artery, and further increase the early contractile response of shock. Antagonized by its specific inhibitor. Conclusion RhoA or Rac agonist or antagonist can regulate the biphasic changes of vascular reactivity in hemorrhagic shock rats, suggesting that RhoA activity is increased and Rac activity is decreased in early shock, while the RhoA activity is decreased and Rac activity is increased in RhoA / The Rac activity balance is involved in the regulation of vasoreactive biphasic changes after shock.