Hiltebrand Luzius B, Krejci Vladimir, Jakob Stephan M, Takala Jukka, Sigurdsson Gisli H
Department of Anesthesia, University of Bern, Inselspital, Bern, Switzerland, and Department of Anesthesia and Intensive Care Medicine, Landspitali University Hospital, Reykjavik, Iceland.
Anesthesiology. 2007 Jun;106(6):1156-67. doi: 10.1097/01.anes.0000267599.02140.86.
Vasopressin increases arterial pressure in septic shock even when alpha-adrenergic agonists fail. The authors studied the effects of vasopressin on microcirculatory blood flow in the entire gastrointestinal tract in anesthetized pigs during early septic shock.
Thirty-two pigs were intravenously anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n=8 in each; full factorial design). Group S (sepsis) and group SV (sepsis-vasopressin) were made septic by fecal peritonitis. Group C and group V were nonseptic control groups. After 300 min, group V and group SV received intravenous infusion of 0.06 U.kg.h vasopressin. In all groups, cardiac index and superior mesenteric artery flow were measured. Microcirculatory blood flow was recorded with laser Doppler flowmetry in both mucosa and muscularis of the stomach, jejunum, and colon.
While vasopressin significantly increased arterial pressure in group SV (P<0.05), superior mesenteric artery flow decreased by 51+/-16% (P<0.05). Systemic and mesenteric oxygen delivery and consumption decreased and oxygen extraction increased in the SV group. Effects on the microcirculation were very heterogeneous; flow decreased in the stomach mucosa (by 23+/-10%; P<0.05), in the stomach muscularis (by 48+/-16%; P<0.05), and in the jejunal mucosa (by 27+/-9%; P<0.05), whereas no significant changes were seen in the colon.
Vasopressin decreased regional flow in the superior mesenteric artery and microcirculatory blood flow in the upper gastrointestinal tract. This reduction in flow and a concomitant increase in the jejunal mucosa-to-arterial carbon dioxide gap suggest compromised mucosal blood flow in the upper gastrointestinal tract in septic pigs receiving low-dose vasopressin.
即使α-肾上腺素能激动剂无效,血管加压素仍可升高感染性休克患者的动脉压。作者研究了血管加压素对麻醉猪早期感染性休克期间整个胃肠道微循环血流的影响。
32头猪静脉麻醉、机械通气,随机分为四组(每组n = 8;完全析因设计)。S组(脓毒症组)和SV组(脓毒症-血管加压素组)通过粪便性腹膜炎造成脓毒症。C组和V组为非脓毒症对照组。300分钟后,V组和SV组静脉输注0.06 U·kg·h血管加压素。所有组均测量心指数和肠系膜上动脉血流量。用激光多普勒血流仪记录胃、空肠和结肠黏膜及肌层的微循环血流。
虽然血管加压素使SV组动脉压显著升高(P<0.05),但肠系膜上动脉血流量下降了51±16%(P<0.05)。SV组全身和肠系膜氧输送及消耗减少,氧摄取增加。对微循环的影响非常不均一;胃黏膜血流下降(23±10%;P<0.05),胃肌层血流下降(48±16%;P<0.05),空肠黏膜血流下降(27±9%;P<0.05),而结肠未见明显变化。
血管加压素使肠系膜上动脉局部血流及上消化道微循环血流减少。血流减少以及空肠黏膜与动脉二氧化碳差值增加提示接受小剂量血管加压素的脓毒症猪上消化道黏膜血流受损。