title: Arginine vasopressin during sinus rhythm: effects on haemodynamic variables, left anterior descending coronary artery cross sectional area and cardiac index, before and after inhibition of NO-synthase, in pigs.
abstract: We have shown previously that arginine vasopressin (AVP) given during sinus rhythm increases mean arterial blood pressure (MAP) and left anterior descending (LAD) coronary artery cross sectional area. AVP was assumed to result in vasodilatation via activation of the endothelial nitric oxide system. The purpose of the present study was to assess the effects of AVP before and after NO-inhibition. Nine domestic pigs were instrumented for measurement of haemodynamic variables using micromanometer-tipped catheters, and measurement of LAD coronary artery cross sectional area employing intravascular ultrasound (IVUS). Haemodynamic variables, LAD coronary artery cross sectional area and cardiac output were measured at baseline, 90 s and 5, 15, and 30 min after AVP (0.4 U kg (-1) IV) before and after blockade of nitric oxide synthase with N(G)-nitro L-arginine methyl ester (L-NAME). Compared with baseline, AVP significantly increased MAP after 90 s (89+/-4 versus 160+/-5 mm Hg), increased LAD coronary artery cross sectional area (11.3+/-1 versus 11.8+/-1 mm(2)) and decreased cardiac index (138+/-6 versus 53+/-6 mL/min kg(-1)). After blockade of nitric oxide synthase, AVP significantly increased MAP after 90 s (135+/-4 versus 151+/-3 mm Hg), increased LAD coronary artery cross sectional area (8.7+/-1 versus 8.9+/-1 mm(2)), and significantly decreased cardiac index (95+/-6 versus 29+/-4 mL/min kg (-1)).
  
  
  CONCLUSIONS
  During sinus rhythm, AVP increased MAP and LAD coronary artery cross sectional area, but decreased cardiac index.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. viktoria.mayr@uibk.ac.at
authors.forename: Viktoria D
authors.initials: VD
authors.lastname: Mayr
authors.forename: Volker
authors.initials: V
authors.lastname: Wenzel
authors.forename: Horst G
authors.initials: HG
authors.lastname: Wagner-Berger
authors.forename: Karl H
authors.initials: KH
authors.lastname: Stadlbauer
authors.forename: Erol
authors.initials: E
authors.lastname: Cavus
authors.forename: Helmut
authors.initials: H
authors.lastname: Raab
authors.forename: Tilko H D
authors.initials: TH
authors.lastname: Müller
authors.forename: Stefan
authors.initials: S
authors.lastname: Jochberger
authors.forename: Martin W
authors.initials: MW
authors.lastname: Dünser
authors.forename: Anette C
authors.initials: AC
authors.lastname: Krismer
authors.forename: Severin
authors.initials: S
authors.lastname: Schwarzacher
authors.forename: Karl H
authors.initials: KH
authors.lastname: Lindner
mesh_terms: D019412:Anatomy, Cross-Sectional; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000187:drug effects* / Q000378:metabolism; D004195:Disease Models, Animal; D006323:Heart Arrest / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D007275:Injections, Intravenous; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D013552:Swine; D018084:Ultrasonography, Interventional; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014693:Ventricular Fibrillation / Q000150:complications / Q000503:physiopathology
chemical_list: D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin; D019001:Nitric Oxide Synthase