Abstract
Sprague–Dawley rats were pretreated with whole body hyperthermia (rectal 42 °C) for 15 min, 24 h before the experiments, and then the left main coronary artery of rat hearts was subjected to a 60 min occlusion followed by 3 h reperfusion. Myocardium injury degree was evaluated by measurement of infarct size and serum creatine kinase (CK) activity. Plasma concentrations of calcitonin gene-related peptide (CGRP), and the expression of α- and β-CGRP mRNA in dorsal root ganglia were determined by radioimmunoassay and semi-quantitative reverse-transcription polymerase chain reaction, respectively. Hyperthermia treatment significantly reduced infarct size and CK release concomitantly with a dramatic increase in plasma concentrations of CGRP and the expression of α-CGRP mRNA, but not β-CGRP mRNA, which was completely abolished by pretreatment with capsazepine (38 mg/kg, s.c.), a competitive vanilloid receptor 1 antagonist. These results suggests that vanilloid receptor 1 on capsaicin-sensitive sensory nerves plays an important role in the modulation of the delayed cardioprotection induced by heat stress in rats.
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