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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/H1702    most recent 00892.2004v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Konrad, D. Articles by Haney, M. Search for Related Content PubMed PubMed Citation Articles by Konrad, D. Articles by Haney, M.

Positive inotropic and negative lusitropic effects of endothelin receptor agonism in vivo

¹Department of Surgical Sciences, Section for Anaesthesiology and Intensive Care, Karolinska Institute, Stockholm; and ²Perioperative and Surgical Sciences, Anesthesiology and Intensive Care Medicine, Umeå University, Umeå, Sweden

Submitted 30 August 2004 ; accepted in final form 31 May 2005

The endothelin (ET) system is involved in the regulation of myocardial function in health as well as in several diseases, such as congestive heart failure, myocardial infarction, and septic myocardial depression. Conflicting results have been reported regarding the acute contractile properties of ET-1. We therefore investigated the effects of intracoronary infusions of ET-1 and of the selective ET_B receptor-selective agonist sarafotoxin 6c with increasing doses in anesthetized pigs. Myocardial effects were measured through analysis of the left ventricular pressure-volume relationship. ET-1 elicited increases in the myocardial contractile status (end-systolic elastance value of 0.94 ± 0.11 to 1.48 ± 0.23 and preload recruitable stroke work value of 68.7 ± 4.7 to 83.4 ± 7.2) that appear to be mediated through ET_A receptors, whereas impairment in left ventricular isovolumic relaxation ( = 41.5 ± 1.4 to 58.1 ± 5.0 and t_1/2 = 23.0 ± 0.7 to 30.9 ± 2.6, where is the time constant for pressure decay and t_1/2 is the half-time for pressure decay) was ET_B receptor dependent. In addition, intravenous administration of ET-1 impaired ventricular relaxation but had no effect on contractility. Intracoronary sarafotoxin 6c administration caused impairments in left ventricular relaxation ( from 43.3 ± 1.8 to 54.4 ± 3.4) as well as coronary vasoconstriction. In conclusion, ET-1 elicits positive inotropic and negative lusitropic myocardial effects in a pig model, possibly resulting from ET_A and ET_B receptor activation, respectively.

cardiac; inotropy; end-systolic elastance; diastolic; porcine; sarafotoxin

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