Ljungdahl M, Rasmussen I, Raab Y, Hillered L, Haglund U
Department of Surgery, University Hospital, Uppsala, Sweden.
Shock. 1997 Feb;7(2):131-8. doi: 10.1097/00024382-199702000-00009.
The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.
本研究旨在利用张力测定法和肠段灌注技术,在猪的缺血/再灌注和脓毒症模型中研究黏膜pH值和乳酸生成情况。18头猪(体重17 - 23千克)接受麻醉并进行机械通气。它们被分为三组,观察4小时。C组(n = 6)作为对照组。在缺血/再灌注组(I/R;n = 6)中,肠系膜上动脉完全阻断60分钟。在P组(n = 6)中,通过粪便性腹膜炎诱导脓毒症。采用热稀释法测定心脏指数(CI),并使用Transonic血流探头测定肠系膜上动脉血流量(QSMA)。使用张力测定法计算黏膜内pH值(pHi)。在回肠中部插入一根用于分段灌注的特殊球囊导管以测量乳酸。测量动脉血和肠系膜上静脉中的乳酸和氧饱和度。对照组中,CI、QSMA、pHi以及血液和灌注液中的乳酸保持不变。肠道血流阻断导致pHi从7.28±0.02降至6.76±0.04,灌注液中乳酸显著升高,动静脉乳酸差值增大。再灌注期间,pHi趋于恢复至基线值。灌注液中的乳酸和动静脉乳酸差值降低。在脓毒症中,CI和QSMA持续降低,分别降至基线的45±13%和40±20%。pHi从7.22±0.09适度降至6.98±0.25。血液和灌注液中的乳酸保持不变。在所有经历缺血/再灌注的动物以及P组6头猪中的3头中观察到微观黏膜损伤。在缺血/再灌注中,pHi与乳酸生成之间存在良好的相关性。然而,在脓毒症中,尽管pHi下降,但肠系膜上静脉血或肠灌注液中的乳酸并未增加。脓毒症和动脉阻塞引起的缺血导致黏膜损伤的机制具有不同特点。