中文摘要：

目的观察RhoA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，取离体血管环和原代血管平滑肌细胞（VSMC），观察在休克不同时期血管反应性的变化以及RhoA活性调节剂对失血性休克后大鼠离体血管环和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，其Emax和60min累计渗透率分别为（1．684±0．101）g／mg组织和68．99±6．83，RhoA的激动剂U46619可进一步升高休克早期或短暂缺氧后血管反应性，RhoA特异性抑制剂C3enzyme可明显降低休克早期和短暂缺氧所引起的血管收缩反应性的升高，其Emax和60min累计渗透率分别为（0．736±0．112）g/mg组织和53．91±5．53。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，其Emax和60min累计渗透率分别为（0．608±0．045）g／mg组织和38．53±4．87，RhoA激动剂U46619可明显升高休克晚期或长时间缺氧所致血管反应性的降低，Emax和60min累计渗透率分别为（0．934±0．110）g／mg组织和57．99±6．83，U-46619的这一作用可被RhoA抑制剂C3enzyme所拮抗。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，RhoA参与了休克血管反应性的调节。

英文摘要：

Objective To observe the effects of RhoA on vascular reactivity following hemorrhagic shock （HS） in rats. Methods The superior mesenteric artery （SMA） from HS rats was adopted to assay the vascular reactivity via observing the contraction initiated with norepinephrine （NE） by isolated organ perfusion system. With transwell culture, the contractile response of Vascular smooth muscle cell （VSMC） to NE 10 or 90 rain after hypoxia was detected. Meanwhile, the effect of the U-46619 and C3enzyme, RhoA activity regulating agents, on vascular reactivity was observed. Results As compared with the control group, the cumulative dose-response curves of SMA to NE at early shock （ immediate after shock） shifted to the left, and the maximal contractions （Emax） of NE was （1. 684 ± 0. 101 ） g/mg tissue and increased significantly. The contractile response of VSMC to NE was increased at 10 min after hypoxia,RhoA agonist U-46619 （10 s mol/L） further increased the contractile response of SMA and VSMC to NE, and C3enzyme decreased reactivity at early shock or 10 min after hypoxia. The cumulative dose-re- sponse curves of SMA to NE at 2 h after shock shifted to the fight, Emax of NE was （0.608 ± 0.045 ） g/ mg tissue and decreased significantly, and the contractile response of VSMC to NE was decreased at 90 min after hypoxia. RhoA agonist U-46619 could increase the vascular reactivity in the late period of shock or at 90 min after hypoxia,and C3enzyme abolished U-46619-induced the increase of the contractile response of SMA and VSMC to NE. Conclusion Vascular reactivity is biphasic change following HS. RhoA may take part in the regulation of biphasic vascular reactivity regulation after HS.