HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Novella, S. Articles by Benedito, S. Search for Related Content PubMed PubMed Citation Articles by Novella, S. Articles by Benedito, S. Related Collections Cardiac - pharmacology Coronary disease Extracorporeal circulation Great vessels

Eur J Cardiothorac Surg 2007;32:69-76. doi:10.1016/j.ejcts.2007.03.047
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Plasma levels and vascular effects of vasopressin in patients undergoing coronary artery bypass grafting

^a Departamento de Fisiología, Facultad de Farmacia, Universidad Complutense, 28040 Madrid, Spain
^b Departamento de Cirugía Cardiovascular, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain

Received 15 January 2007; received in revised form 29 March 2007; accepted 30 March 2007.

^_* Corresponding author. Address: Sección Departamental de Fisiología, Facultad de Farmacia, Universidad Complutense, 28040 Madrid, Spain. Tel.: +34 91 394 1696; fax: +34 91 394 1696. (Email: sbenedi{at}farm.ucm.es).

Objective: Recent studies have suggested that endogenous vasopressin (AVP) acts as a spasmogen during coronary artery bypass grafting (CABG). Given that AVP could induce vasospasm in the grafted vessel, we assessed the release of this peptide during and after CABG, and explored ways of counteracting its contractile effect on the internal mammary artery (IMA). Methods: Plasma levels of AVP were determined by radioimmunoassay in 16 patients before, during and after CABG. Using isometric force recording techniques, we also investigated the mechanisms involved in the contractile effect of AVP in ring preparations of IMA specimens taken from 95 patients. Results: Plasma AVP levels peaked after the start of cardiopulmonary bypass (CPB) and correlated well with serum osmolality (Pearson's r = 0.9490; P < 0.0001; n = 16). An inverse correlation was observed between plasma AVP levels recorded at this stage and the maximal contraction induced in vitro by AVP in vascular rings from the same patients (Pearson's r = –0.6968; P < 0.01; n = 16). No change in the AVP response was produced by endothelium removal, exposure to the NO precursor (3 x 10^–4 M L-arginine), inhibition of nitric oxide (NO) synthase (3 x 10^–5 M L-NAME) or soluble guanylate cyclase (3 x 10^–6 M 1H-[1,2,4]oxadiazol [4,3,-]quinoxalin-1-one (ODQ)), removal of the superoxide anion (100 U/ml superoxide dismutase (SOD) plus 1200 U/ml catalase) or hydroxyl radical (10^–4 M deferoxamine), or specific ₁- (10^–6 M prazosin) or endothelin (10^–5 M bosentan) receptor antagonism. In contrast, adenylate cyclase activation (3 x 10^–8 M forskolin) reduced the contractile response to AVP, while prostanoid synthesis (3 x 10^–6 M indomethacin) inhibition and blockade of Ca²⁺-activated potassium channels (K_Ca) (10^–3 M tetraethylammonium (TEA)) enhanced AVP contraction. Age, gender and smoking also modified the AVP response. Conclusion: Our findings suggest a role for AVP as a modulator of vascular tone in human IMA. The effect of AVP is dependent on prostanoids and Ca²⁺-activated K⁺ channels, so its dysfunction in pathophysiological cardiovascular processes could mean that AVP, among other factors, produces vasospasm in IMA grafts.

Key Words: Coronary artery bypass grafting • Vasopressin • Vasospasm • Internal mammary artery