Shin C S, Lee K Y, Kim J L, Lee H W, Schenarts P J, Traber D L
Department of Anesthesiology, Yonsei University College of Medicine, Seoul, Korea.
Yonsei Med J. 1997 Jun;38(3):142-50. doi: 10.3349/ymj.1997.38.3.142.
It has already been shown that pulmonary injury is induced after intestinal or hind limb ischemia-reperfusion injury. The purpose of this study was to determine the effect of renal ischemia-reperfusion injury on the pulmonary system. We compared the pulmonary effects of 60 and 90 minutes ischemia followed by 24 hour reperfusion in sheep kidneys. Standard hemodynamic measurements, arterial and mixed venous blood gas analysis, urine output, creatinine clearance, and blood urea nitrogen concentration were measured at baseline, during ischemia and reperfusion periods. After 24 hours of reperfusion, animals were sacrificed and underwent autopsy with collection of samples for wet/dry lung-weight ratio, lung tissue conjugated dienes, and renal histology. As expected, renal ischemia resulted in an increased serum creatinine and blood urea nitrogen concentrations, decreased creatinine clearance, and histological evidence of renal damage. There was no evidence of pulmonary hypertension or hypoxemia during renal ischemia-reperfusion. There was also no significant difference in the wet/dry lung-weight ratios or lung tissue conjugated denies between the two ischemic groups (60 and 90 minutes) and nonischemic control group. These results suggest that renal ischemia-reperfusion injury was not associated with a significant degree of pulmonary dysfunction.
业已表明，肠道或后肢缺血再灌注损伤后会引发肺损伤。本研究的目的是确定肾缺血再灌注损伤对肺系统的影响。我们比较了绵羊肾脏60分钟和90分钟缺血后再灌注24小时对肺的影响。在基线、缺血期和再灌注期测量标准血流动力学指标、动脉血和混合静脉血气分析、尿量、肌酐清除率以及血尿素氮浓度。再灌注24小时后，处死动物并进行尸检，收集样本以测定肺湿/干重比、肺组织共轭二烯以及肾脏组织学情况。不出所料，肾缺血导致血清肌酐和血尿素氮浓度升高、肌酐清除率降低以及肾脏损伤的组织学证据。肾缺血再灌注期间没有肺动脉高压或低氧血症的证据。两个缺血组（60分钟和90分钟）与非缺血对照组之间的肺湿/干重比或肺组织共轭二烯也没有显著差异。这些结果表明，肾缺血再灌注损伤与显著程度的肺功能障碍无关。
