Welte M, Pichler B, Groh J, Anthuber M, Jauch K W, Pratschke E, Lenhart F P, Haller M, Frey L, Peter K
Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München, Germany.
Br J Anaesth. 1996 Jan;76(1):90-8. doi: 10.1093/bja/76.1.90.
Although impairment of splanchnic perfusion may induce mucosal hypoxia and endotoxaemia during orthotopic liver transplantation (OLT), little is known about the changes in mucosal oxygenation during and after the procedure. To study the effects of liver surgery itself on mucosal pH (pHi) and the response of pHi to acute changes in portal flow, we measured gastric pHi during six liver resections using tonometry: in two patients, after clamping of the hepatoduodenal ligament, pHi decreased within 30 min and recovered promptly after reperfusion. We then investigated gastric and sigmoid pHi (pHig, pHis) during the perioperative phase in 18 OLT. Median pHi values were low before surgery (pHig 7.28 (first/third quartiles 7.22/7.34); pHis 7.27 (7.12/7.36)). Although global oxygen delivery and haemodynamic variables remained constant and veno-venous bypass (VVB) was used to maintain portal flow, pHi declined during the anhepatic phase (pHig 7.19 (7.13/7.23), P < 0.01; pHis 7.13 (7.06/7.24), P < 0.05). After reperfusion of the graft, pHi recovered and did not differ from baseline values by the end of OLT. After operation pHig increased further, reaching the highest values 30 h after ICU admission (7.34 (7.26/7.38)). In the intraoperative period, no significant endotoxaemia was observed either in portal or systemic blood. The maximum reduction in pHi was related neither to the duration of VVB and OLT nor to the number of red cell units transfused. pHi after reperfusion did not correlate with graft viability or dysfunction of the lung or kidney. We conclude that pHi indicates mucosal ischaemia during OLT which is not necessarily associated with endotoxaemia, and intraoperative pHi monitoring does not appear to be a valuable predictor of postoperative graft failure and organ dysfunction.
尽管在原位肝移植（OLT）过程中内脏灌注受损可能会导致黏膜缺氧和内毒素血症，但对于该手术期间及术后黏膜氧合的变化却知之甚少。为了研究肝脏手术本身对黏膜pH值（pHi）的影响以及pHi对门静脉血流急性变化的反应，我们使用张力测定法在6例肝脏切除术期间测量了胃pHi：在2例患者中，肝十二指肠韧带夹闭后，pHi在30分钟内下降，并在再灌注后迅速恢复。然后，我们在18例OLT的围手术期研究了胃和乙状结肠的pHi（pHig，pHis）。术前pHi的中位数较低（pHig 7.28（第一/第三四分位数7.22/7.34）；pHis 7.27（7.12/7.36））。尽管全身氧输送和血流动力学变量保持恒定，且使用静脉-静脉转流（VVB）来维持门静脉血流，但在无肝期pHi仍下降（pHig 7.19（7.13/7.23），P<0.01；pHis 7.13（7.06/7.24），P<0.05）。移植肝再灌注后，pHi恢复，到OLT结束时与基线值无差异。术后pHig进一步升高，在重症监护病房（ICU）入院后30小时达到最高值（7.34（7.26/7.38））。在手术期间，门静脉或全身血液中均未观察到明显的内毒素血症。pHi的最大降幅既与VVB和OLT的持续时间无关，也与输注的红细胞单位数量无关。再灌注后的pHi与移植肝的活力或肺或肾的功能障碍无关。我们得出结论，pHi表明OLT期间存在黏膜缺血，这不一定与内毒素血症相关，并且术中pHi监测似乎不是术后移植肝失败和器官功能障碍的有价值预测指标。
