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Ethanol preconditioning protects against ischemia/reperfusion‐induced cardiac damage via calcitonin gene‐related peptide and is initiated by a transient receptor potential vanilloid 1‐dependent mechanism
Author(s) -
Wang Meifang,
Zuidema Mozow Y.,
Korthuis Ronald J.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.678.5
Subject(s) - calcitonin gene related peptide , trpv1 , capsazepine , ischemia , chemistry , reperfusion injury , medicine , troponin i , pharmacology , endocrinology , ethanol , receptor , anesthesia , transient receptor potential channel , neuropeptide , biochemistry , myocardial infarction
Our previous studies indicated that ingestion of ethanol at low to moderate levels prior to ischemia/reperfusion (I/R) protects against postischemic intestinal and cerebral injury. These protective actions are initiated by a calcitonin gene‐related peptide (CGRP)/ transient receptor potential vanilloid 1 (TRPV1) ‐ dependent mechanism. This study was to determine whether a similar mechanism underlies the protective effect of ethanol preconditioning in cardiac I/R injury. Serum Troponin‐I (cTnI), a marker of myocardial injury, was markedly elevated in wild type male C57BL/6J mice after 30 min left anterior descending (LAD) ischemia and 4 h reperfusion, at which cTnI reaches its peak level. When mice were treated with ethanol 24 h prior to cardiac I/R as a bolus by gavage (at a dose that produces peak plasma ethanol of 40–45 mg/dl), cTnI levels did not increase in comparison to I/R alone (p<0.001). This protective effect of ethanol consumption was significantly attenuated by administration of capsazepine, a competitive TRPV1 antagonist 10 min before ethanol ingestion (p<0.05). These findings demonstrate the protection against cardiac I/R from antecedent ethanol ingestion occurs via a TRPV1‐dependent mechanism. Supported by a grant from the NIH (AA‐014945).