Endothelin-1 and myocardial preconditioning

J. M. Erikson, C. E. Velasco

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

This study attempted to define the role of endothelin (ET) in preconditioning. We previously showed that ET is produced during myocardial ischemia and reperfusion. Because both preconditioning and ET act through protein kinase C, ET could play a role in preconditioning. Dogs were randomized to three groups subjected to 40 minutes of ischemia, with (groups A and B) or without (group C) preconditioning, followed by 4 hours of reperfusion. Groups A and C received saline infusions; group B received continuous infusions of the ET(A)-selective antagonist FR 139317. Both preconditioned groups had smaller infarct sizes (group A, 7.9% ± 2.5%; group B, 8.4% ± 2.6%) than the nonpreconditioned group (group C, 16.2% ± 3.3%). Administration of the ETA antagonist FR139317 did not alter infarct size. This study demonstrated that ET(A)-receptor blockade did not alter infarct size in preconditioned animals and suggests that endothelin does not play a significant role in this process.

Original languageEnglish (US)
Pages (from-to)84-90
Number of pages7
JournalAmerican heart journal
Volume132
Issue number1 I
DOIs
StatePublished - Jan 1 1996

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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