Li Tao, Liu Liang-ming, Yang Guang-ming, Xu Jing, Ming Jia
State Key Laboratory of Trauma, Burns and Combined Injury, Department Two, Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing 400042, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 Nov;17(11):647-50.
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.
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.
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).
Sensitivity of vascular smooth muscle to calcium following hemorrhagic displays a biphasic change. It plays important roles in biphasic vascular reactivity.
观察大鼠失血性休克（HS）后血管平滑肌对钙的敏感性变化及其在血管双相反应性中的作用。
采用HS大鼠的肠系膜上动脉（SMA），通过离体器官灌流系统观察去甲肾上腺素（NE）和Ca²⁺在去极化条件（120 mmol/L K⁺）下引发的收缩，测定血管反应性和对钙的敏感性。在休克后的不同时间点，分析血管反应性与对钙敏感性之间的关系。同时观察钙敏感性调节剂血管紧张素II（Ang II）和胰岛素对血管反应性的影响。
与对照组相比，休克早期即休克即刻和休克后30分钟时，SMA对NE和Ca²⁺的累积剂量 - 反应曲线左移，NE和Ca²⁺的最大收缩力（Emax）显著增加（P<0.05或P<0.01）。但休克后期SMA对NE和Ca²⁺的累积剂量 - 反应曲线右移，NE和Ca²⁺的Emax显著降低（P<0.05或P<0.01）。休克持续2小时时，Ang II增加了SMA对NE和Ca²⁺的收缩反应，使NE和Ca²⁺的累积剂量 - 反应曲线左移（P<0.05或P<0.01）。但休克早期胰岛素降低了SMA对NE和Ca²⁺的收缩反应，使NE和Ca²⁺的累积剂量 - 反应曲线右移（P<0.05或P<0.01）。
失血性休克后血管平滑肌对钙的敏感性呈现双相变化。它在血管双相反应性中起重要作用。
