Objective: To observe the change in sensitivity of vascular smooth muscle to calcium and its role in biphasic vascular reactivity following hemorrhagic shock (HS) in rats.
Methods: The superior mesenteric artery (SMA) obtained from rats with HS was used to assay the vascular reactivity and sensitivity to calcium by observing the contraction initiated by norepinephrine (NE) and Ca(2+) under depolarizing conditions (120 mmol/L K(+)) with isolated organ perfusion system. At different time points after shock, the relationship between vascular reactivity and sensitivity to calcium was analyzed. Meanwhile the effects of the angiotensin II (Ang II) and insulin, the calcium sensitivity regulating agents, on vascular reactivity were also observed.
Results: As compared with the control group, the cumulative dose-response curves of SMA to NE and Ca(2+) at early shock stages, i.e. immediately and 30 minutes after shock, shifted to the left, the maximal contractions (Emax) of NE and Ca(2+) were increased significantly (P<0.05 or P<0.01). But the cumulative dose-response curves of SMA to NE and Ca(2+) at late shock stage shifted to the right, and Emax of NE and Ca(2+) were significantly decreased (P<0.05 or P<0.01). Ang II increased the contractile response of SMA to NE and Ca(2+) when shock persisted for 2 hours, rendering the cumulative dose-response curves of NE and Ca(2+) shifted to the left (P<0.05 or P<0.01). But insulin decreased the contractile response of SMA to NE and Ca(2+) at early stage of shock, rendering the cumulative dose-response curves of NE and Ca(2+) shifted to the right (P<0.05 or P<0.01).
Conclusion: Sensitivity of vascular smooth muscle to calcium following hemorrhagic displays a biphasic change. It plays important roles in biphasic vascular reactivity.