The Effects of Rac on Vascular Reactivity Following Hemorrhagic Shock in Rats
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Graphical Abstract
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Abstract
OBJECTIVE To observe the effects of Rac on vascular reactivity following hemorrhagic shock(HS) in rats. METHODS The superior mesenteric artery(SMA) from hemorrhagic shock rats was adopted to assay the vascular reactivity via observing the contraction initiated by norepinephrine(NE) with isolated organ perfusion system. With transwell culture, the contractile response of VSMC to NE after hypoxia (10 min, 90 min, after hypoxia). Meanwhile, the effect of the PDGF and NSC 23766, Rac activity regulating agents, on vascular reactivity was observed. RESULTS The contractile response of SMA to NE at early shock( immediate after shock) and VSMC contractility to NE after transient hypoxia (10min after hypoxia) were significantly increased, Rac agonist PDGF the decreased reactivity of SMA and VSMC to NE at early shock or 10 min after hypoxia. The effect of PDGF was abolished by NSC 23766. But in the late period of shock or after prolonged hypoxia, the contractile response of SMA and VSMC to NE was decreased, Rac agonist PDGF had no influence on decreasing vascular reactivity in the later period of shock or after 90 min hypoxia, while its inhibitor NSC 23766 increased the contractile response of SMA and VSMC to NE. CONCLUSION Vascular reactivity is biphasic change following hemorrhagic shock, Rac takes part in the regulation of biphasic vascular reactivity regulation after shock.
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