Low-dose terlipressin during long-term hyperdynamic porcine endotoxemia:: Effects on hepatosplanchnic perfusion, oxygen exchange, and metabolism

被引:61
作者
Asfar, P [1 ]
Hauser, B
Iványi, Z
Ehrmann, U
Kick, J
Albicini, M
Vogt, J
Wachter, U
Brückner, UB
Radermacher, P
Bracht, H
机构
[1] Sekt Anasthesiol Pathophysiol & Verfahrensentwick, Ulm, Germany
[2] CHU, Serv Reanimat Med, Angers, France
[3] Semmelweis Egyetem, Aneszteziol Intenz Terapias Klin, Budapest, Hungary
[4] Univ Ulm Klinikum, Abt Thorax & Gefasschirurg, D-7900 Ulm, Germany
[5] Univ Milan, Ist Anesthesiol & Rianimaz, Milan, Italy
[6] Polo Univ San Paolo, Azienda Osped, Milan, Italy
[7] Univ Ulm Klinikum, Sekt Chirurg Forsch, D-7900 Ulm, Germany
关键词
vasopressin analog; hepatic arterial buffer response; microcirculation; endogenous glucose production; lactate; pyruvate;
D O I
10.1097/01.CCM.0000152253.45901.FB
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objective: To investigate whether the vasopressin analog terlipressin might induce hepatosplanchnic ischemia during long-term, hyperdynamic, volume-resuscitated porcine endotoxemia. Design: Prospective, randomized, controlled experimental study with repeated measures. Setting: Investigational animal laboratory. Subjects: Eighteen pigs were divided into two groups receiving either endotoxin alone (control group, n = 10) or endotoxin and terlipressin (n = 8). Interventions: Pigs were anesthetized, mechanically ventilated, and instrumented and received a continuous intravenous infusion of Escherichia coli endotoxin. Animals were resuscitated with hydroxyethyl starch targeted to maintain mean arterial pressure > 60 mm Hg. Twelve hours after the start of the endotoxin infusion, terlipressin (5-15 mug(.)kg(-1.)hr(-1) titrated to maintain mean arterial pressure at preendotoxin levels) or its vehicle was administered for 12 hrs. Measurements and Main Results: Terlipressin increased mean arterial pressure and systemic vascular resistances, which was affiliated with a decrease in cardiac output and global oxygen consumption. Terlipressin restored the hepatic artery buffer response, which led to an increase in hepatic artery flow, ultimately resulting in well-maintained liver oxygen delivery, oxygen uptake, and all other variables of regional metabolism and organ function. Terlipressin markedly attenuated the hepatosplanchnic venous acidosis but was associated with pronounced hyperlactatemia. Conclusions: During long-term hyperdynamic porcine endotoxemia, the well-known vasoconstrictor properties of terlipressin blunted the progressive decrease in mean arterial pressure without any detrimental effect on hepatosplanchnic perfusion, oxygen exchange, and metabolism. The marked terlipressin-induced hyperlactaternia did not originate from the hepatosplanchnic organs but from extrasplanchnic tissues, possibly muscle and skin.
引用
收藏
页码:373 / 380
页数:8
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