Suzuki H, Robinson M K, Rounds J D, Gatzen C, Wilmore D W
Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts.
J Surg Res. 1994 Nov;57(5):632-9. doi: 10.1006/jsre.1994.1193.
Liver ischemia-reperfusion is known to be associated with free radical-mediated hepatocellular damage but alterations in hepatocellular fluid flux under these conditions are incompletely understood. Deficiency of the antioxidant glutathione, which increases the liver's susceptibility to ischemia-reperfusion injury, may exacerbate pathological fluid shifts. This study examined alterations in hepatic fluid dynamics during liver ischemia-reperfusion in glutathione-deficient and glutathione-replete rats. Normal and glutathione-deficient rats underwent liver ischemia-reperfusion. Changes in hepatic extra- and intracellular fluid were monitored by calculating extra- and intracellular conductance from liver multifrequency bioelectrical impedance measurements. Liver malonyl dialdehyde content and plasma transaminase concentrations were measured and correlated with changes in hepatic impedance. Hepatic extracellular conductance decreased during ischemia and returned toward baseline values during reperfusion in a similar fashion in both study groups. Intracellular conductance increased during ischemia in both groups and continued to rise during the initial phase of reperfusion before falling toward normal. Glutathione-deficient rats had a significantly higher intracellular conductance during early reperfusion compared to controls. Glutathione-depleted rats also had higher serum transaminases and liver malonyl dialdehyde content following reperfusion. Intracellular and extracellular conductance were significantly correlated with hepatic malonyl dialdehyde content. We conclude that (1) liver ischemia-reperfusion results in movement of fluid from the extracellular to intracellular space with hepatocellular swelling; (2) glutathione deficiency accentuates hepatocyte swelling following ischemia-reperfusion; and (3) changes in extra- and intracellular fluid are related to the severity of membrane damage.(ABSTRACT TRUNCATED AT 250 WORDS)
肝脏缺血再灌注与自由基介导的肝细胞损伤相关，但在这些情况下肝细胞液体通量的变化尚未完全明确。抗氧化剂谷胱甘肽缺乏会增加肝脏对缺血再灌注损伤的易感性，可能会加剧病理性液体转移。本研究检测了谷胱甘肽缺乏和谷胱甘肽充足的大鼠在肝脏缺血再灌注期间肝脏液体动力学的变化。正常大鼠和谷胱甘肽缺乏大鼠接受肝脏缺血再灌注。通过肝脏多频生物电阻抗测量计算细胞外和细胞内电导率来监测肝脏细胞外和细胞内液体的变化。测量肝脏丙二醛含量和血浆转氨酶浓度，并将其与肝脏阻抗变化相关联。两个研究组中，肝脏细胞外电导率在缺血期间均下降，再灌注期间以类似方式恢复至基线值。两组中细胞内电导率在缺血期间均增加，并在再灌注初始阶段持续上升，之后降至正常。与对照组相比，谷胱甘肽缺乏的大鼠在再灌注早期细胞内电导率显著更高。再灌注后，谷胱甘肽耗竭的大鼠血清转氨酶和肝脏丙二醛含量也更高。细胞内和细胞外电导率与肝脏丙二醛含量显著相关。我们得出结论：（1）肝脏缺血再灌注导致液体从细胞外空间转移至细胞内空间，伴有肝细胞肿胀；（2）谷胱甘肽缺乏会加剧缺血再灌注后的肝细胞肿胀；（3）细胞外和细胞内液体的变化与膜损伤的严重程度相关。（摘要截短于250字）
