Iwata T, Gilispie A, Jorns C, Yamamoto S, Nowak G, Ericzon B-G
Department for Clinical Science, Intervention and Technology (CLINTEC), Division of Transplantation Surgery, Karolinska Institute, Karolinska University Hospital, Huddinge, B56 141-86, Stockholm, Sweden.
Surg Endosc. 2008 Apr;22(4):938-42. doi: 10.1007/s00464-007-9525-0. Epub 2007 Aug 19.
Laparoscopic donor nephrectomy has become the first choice for living donor kidney transplantation, offering advantages over open donor nephrectomy. This study aimed to evaluate kidney tissue metabolism during and after pneumoperitoneum using a microdialysis technique.
Eight pigs underwent laparotomy and implantation of two microdialysis catheters: one in the cortex and one in the medulla of the left kidney. After laparotomy, the abdominal wall was closed, and pneumoperitoneum was induced with a constant standard pressure of 16 to 18 mmHg for 4 h, followed by rapid desufflation. In microdialysis samples collected from intrarenal catheters, markers of ischemia (glucose, lactate, pyruvate, and lactate-pyruvate ratio) and the marker of cell membrane injury (glycerol) were monitored.
There were no changes in glucose, lactate, or pyruvate level before, during, or after pneumoperitoneum, either in the cortex or in the medulla. Additionally, the calculated lactate-pyruvate ratio did not show signs of ischemia during or after pneumoperitoneum. However, with regard to the marker of cell injury, glycerol increased in the medulla after decompression from 22.57 +/- 3.76 to 35.67 +/- 5.43 mmol/l (p < 0.01). This release of glycerol in the medulla was significantly higher than in the cortex (area under the curve [AUC], 22.18 +/- 4.87 vs 34.79 +/- 7.88 mmol/l; p < 0.01).
The pattern of metabolic changes monitored in the kidney during and after pneumoperitoneum indicates some kind of cell injury predominant in the medulla without any signs of kidney ischemia. This nonischemic injury could be related to hyperperfusion of the kidney after decompression or injury to cells attributable to mechanical cell expansion at the point of rapid decompression.
腹腔镜供肾切除术已成为活体供肾肾移植的首选方法，与开放性供肾切除术相比具有优势。本研究旨在使用微透析技术评估气腹期间及气腹后肾组织的代谢情况。
八头猪接受剖腹手术并植入两根微透析导管：一根置于左肾皮质，一根置于髓质。剖腹手术后，关闭腹壁，以16至18 mmHg的恒定标准压力诱导气腹4小时，然后快速放气。监测从肾内导管收集的微透析样本中缺血标志物（葡萄糖、乳酸、丙酮酸和乳酸 - 丙酮酸比值）以及细胞膜损伤标志物（甘油）。
气腹前、气腹期间和气腹后，皮质或髓质中的葡萄糖、乳酸或丙酮酸水平均无变化。此外，计算得出的乳酸 - 丙酮酸比值在气腹期间和气腹后均未显示缺血迹象。然而，关于细胞损伤标志物，减压后髓质中的甘油从22.57±3.76 mmol/l增加至35.67±5.43 mmol/l（p<0.01）。髓质中甘油的这种释放明显高于皮质（曲线下面积[AUC]，22.18±4.87 vs 34.79±7.88 mmol/l；p<0.01）。
气腹期间及气腹后在肾脏中监测到的代谢变化模式表明，髓质中存在某种以细胞损伤为主的情况，而无任何肾脏缺血迹象。这种非缺血性损伤可能与减压后肾脏的高灌注或快速减压时机械性细胞扩张导致的细胞损伤有关。
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