Vasopressin in vasodilatory shock is the heart in danger 英文参考文献.docVIP

Available online /content/12/2/132 Commentary Vasopressin in vasodilatory shock: is the heart in danger? Balázs Hauser1,4, Pierre Asfar2, Enrico Calzia1, Régent Laporte3, Michael Georgieff1 and Peter Radermacher1 1Sektion An?sthesiologische Pathophysiologie und Verfahrensentwicklung, Universit?tsklinikum, Parkstrasse 11, 89073 Ulm, Germany 2Laboratoire HIFIH UPRES-EA 3859, IFR 132, Université d’Angers, Département de Réanimation Médicale, CHU, 4 rue Larrey, 49993 Angers Cedex 9, France 3Ferring Research Institute Inc, Building 2, Room 439, 3550 General Atomics Court, San Diego, CA 92121, USA 4Present address: Aneszteziológiai és Intenzív Terápiás Klinika, Semmelweis Egyetem, H-1125 Kútv?lgyi út 4, Budapest, Hungary Corresponding author: Peter Radermacher, peter.radermacher@uni-ulm.de Published: 10 April 2008 Critical Care 2008, 12:132 (doi:10.1186/cc6839) This article is online at /content/12/2/132 ? 2008 BioMed Central Ltd See related research by Müller et al., /content/12/1/R20 Abstract mental AVP – similar to the pure α-agonist phenylephrine – dose-dependently reduced organ blood flow [2]. Müller and colleagues unfortunately did not measure portal venous flow, but it is tempting to speculate that the increased hepatic arterial flow reflects a well-maintained hepatic arterial buffer response, which at least partially compensated for the most likely reduced portal venous flow. In fact, low doses of the AVP analogue terlipressin during long-term, hyperdynamic In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow. Depending on the infusion rate, this vasoconstriction also reduces coronary blood flow despite an increased coronary perfusion pressure. In a porcine model of transitory myocardial ischemia-induced left ventricular dysfunction, M