Haglind E, Haglund U, Haljamäe H
Dept. of Surgery I, Sahlgrenska Hospital, University of Göteborg, Sweden.
Res Exp Med (Berl). 1988;188(3):197-207. doi: 10.1007/BF01852321.
The liver metabolic response of rats following a standardized intestinal shock, induced by applying a pressure of 120 cm water on the mesenteric vessels for 60 min, was studied. Immediately prior to the release of the pressure on the vessels saline or naloxone was given either as a single injection or as a continuous infusion. After the reperfusion of the intestine no early disturbances in liver metabolism were found as evidenced from the ATP, glucose and lactate levels in liver biopsies taken 15 min following reflow. Within 60 min of reflow reduction of ATP and increases of glucose and lactate levels occurred. There were no major hemodynamic or liver metabolic differences between saline- and naloxone-treated shocked rats. When saline or naloxone was given as a continuous infusion, the changes in liver metabolism were, however, less severe than those observed in the single injection situation pointing toward a non-specific effect of volume replacement rather than a blockade of opioid receptors. Hepatic hypoxia and/or cellular effects of "shock factors" could be mechanisms of pathophysiologic importance for the disturbed liver metabolism in this shock model.
研究了通过对肠系膜血管施加120厘米水柱压力60分钟诱导的标准化肠休克后大鼠的肝脏代谢反应。在解除血管压力之前，立即单次注射或持续输注生理盐水或纳洛酮。肠再灌注后，从再灌注后15分钟采集的肝脏活检组织中的ATP、葡萄糖和乳酸水平来看，未发现肝脏代谢有早期紊乱。再灌注后60分钟内，ATP减少，葡萄糖和乳酸水平升高。生理盐水和纳洛酮治疗的休克大鼠之间在主要血流动力学或肝脏代谢方面没有差异。然而，当持续输注生理盐水或纳洛酮时，肝脏代谢的变化比单次注射时观察到的要轻，这表明是容量替代的非特异性作用，而非阿片受体阻断作用。肝缺氧和/或“休克因子”的细胞效应可能是该休克模型中肝脏代谢紊乱的重要病理生理机制。
