The effects of RhoA on vascular reactivity following hemorrhagic shock in rats

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. Key words: Shock,hemorrhagic ;  RhoA ;  Vascular