Tugtekin I F, Radermacher P, Theisen M, Matejovic M, Stehr A, Ploner F, Matura K, Ince C, Georgieff M, Träger K
Sektion Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinik für Anästhesiologie, Parkstrasse 11, 89075, Ulm, Germany.
Intensive Care Med. 2001 Apr;27(4):757-66. doi: 10.1007/s001340100871.
To investigate whether an increased ileal-mucosal-arterial PCO2 gap (delta PCO2) during hyperdynamic porcine endotoxemia is associated with impaired villus microcirculation.
Prospective, randomized, controlled, experimental study.
Animal research laboratory.
Twenty-two domestic pigs.
After baseline measurements, anesthetized and ventilated pigs received continuous i.v. endotoxin (ETX, n = 12) for 24 h or placebo (SHAM, n = 10).
Before, as well as 12 and 24 h after, the start of endotoxin or saline portal venous blood flow (QPV, ultrasound flow probe) and lactate/pyruvate ratios (L/P), the ileal-mucosal-arterial delta PCO2 (fiberoptic sensor) and bowel-wall capillary hemoglobin O2 saturation (%Hb-O2-cap, remission spectrophotometry) were assessed together with intravital video records of the ileal-mucosal microcirculation (number of perfused/heterogeneously perfused/unperfused villi) using orthogonal polarization spectral imaging (CYTOSCAN A/R) via an ileostomy. At 12 and 24 h endotoxin infusion, about half of the evaluated villi were heterogeneously or unperfused which was paralleled by a progressive significant increase of the ileal-mucosal-arterial delta PCO2 and portal venous L/P ratios, whereas QPV as well as both the mean %Hb-O2-cap and the %Hb-O2-cap frequency distributions remained unchanged. By contrast, in the SHAM-group, mucosal microcirculation was well-preserved, and none of the other parameters were influenced.
We conclude that an increased ileal-mucosal-arterial delta PCO2 during porcine endotoxemia is related to impaired villus microcirculation. A putative contribution of disturbed cellular oxygen utilization resulting from "cytopathic hypoxia" may also assume importance.
研究在高动力性猪内毒素血症期间,回肠黏膜动脉二氧化碳分压差值(δPCO2)升高是否与绒毛微循环受损有关。
前瞻性、随机、对照实验研究。
动物研究实验室。
22头家猪。
在进行基线测量后,对麻醉并通气的猪持续静脉输注内毒素(ETX,n = 12)24小时或给予安慰剂(假手术组,SHAM,n = 10)。
在内毒素或生理盐水输注开始前、开始后12小时和24小时,使用超声血流探头评估门静脉血流量(QPV)以及乳酸/丙酮酸比值(L/P),使用光纤传感器评估回肠黏膜动脉δPCO2,使用反射分光光度法评估肠壁毛细血管血红蛋白氧饱和度(%Hb - O2 - cap),同时通过回肠造口术,使用正交偏振光谱成像(CYTOSCAN A/R)对回肠黏膜微循环进行活体视频记录(灌注/不均一灌注/未灌注绒毛的数量)。在内毒素输注12小时和24小时时,约一半被评估的绒毛出现不均一灌注或未灌注,与此同时,回肠黏膜动脉δPCO2和门静脉L/P比值逐渐显著升高,而QPV以及平均%Hb - O2 - cap和%Hb - O2 - cap频率分布保持不变。相比之下,在假手术组中,黏膜微循环保存良好,其他参数均未受影响。
我们得出结论,猪内毒素血症期间回肠黏膜动脉δPCO2升高与绒毛微循环受损有关。由“细胞病性缺氧”导致的细胞氧利用紊乱的潜在作用也可能很重要。