Fink M P
Department of Surgery, University of Massachusetts Medical Center, Worcester.
Crit Care Med. 1993 Feb;21(2 Suppl):S4-8. doi: 10.1097/00003246-199302001-00002.
To provide a succinct overview of current notions regarding sepsis-induced alterations in mesenteric perfusion and oxygen transport.
Selected English-language articles dealing with mesenteric perfusion and gut mucosal function during sepsis or endotoxicosis in experimental animals or man.
The review emphasizes findings obtained using a well-characterized porcine model of acute, resuscitated endotoxicosis. Other experimental and clinical studies are discussed as well.
Total hepatosplanchnic perfusion and oxygen uptake are increased in most patients with compensated sepsis. No data are currently available from clinical studies regarding the effect of sepsis on mesenteric perfusion per se. Data are unavailable regarding either total hepatosplanchnic or mesenteric blood flow in patients with decompensated sepsis (i.e., septic shock). Therefore, current ideas regarding mesenteric perfusion in sepsis derive primarily from studies using animal models. In a normodynamic porcine endotoxicosis model, mesenteric perfusion and oxygen delivery (DO2) are markedly decreased. The changes in flow and DO2 are accompanied by intestinal mucosal acidosis and increased permeability to hydrophilic solutes, suggesting that these latter phenomena are a consequence of lipopolysaccharide-induced mesenteric hypoperfusion. This idea is supported by the observation that maintenance of normal mesenteric blood flow ameliorates gut mucosal acidosis and hyperpermeability in endotoxic pigs. However, because transmesenteric oxygen consumption is unchanged in endotoxic pigs, the precise mechanistic relationship between hypoperfusion and altered barrier function remains puzzling.
Mesenteric hypoperfusion may be an important factor leading to alterations in gut epithelial permeability in endotoxicosis and sepsis.
简要概述目前关于脓毒症引起的肠系膜灌注和氧输送改变的观点。
选择有关实验动物或人类脓毒症或内毒素血症期间肠系膜灌注和肠黏膜功能的英文文章。
本综述重点介绍使用特征明确的急性复苏性内毒素血症猪模型获得的研究结果。也讨论了其他实验和临床研究。
大多数代偿性脓毒症患者的全肝脾灌注和氧摄取增加。目前尚无临床研究关于脓毒症对肠系膜灌注本身影响的数据。关于失代偿性脓毒症（即脓毒性休克）患者的全肝脾或肠系膜血流的数据也不可用。因此，目前关于脓毒症中肠系膜灌注的观点主要来自动物模型研究。在正常动力学的猪内毒素血症模型中，肠系膜灌注和氧输送（DO2）明显降低。血流和DO2的变化伴随着肠黏膜酸中毒和对亲水性溶质通透性增加，提示这些现象是脂多糖诱导的肠系膜灌注不足的结果。维持正常肠系膜血流可改善内毒素血症猪的肠黏膜酸中毒和高通透性这一观察结果支持了这一观点。然而，由于内毒素血症猪的跨肠系膜氧消耗未改变，灌注不足与屏障功能改变之间的确切机制关系仍不清楚。
肠系膜灌注不足可能是导致内毒素血症和脓毒症中肠上皮通透性改变的重要因素。
