The Role of Cannabinoid Receptors and TRPV1 Channel in the Infarct‐Reducing Effect of Cold Adaptation

An increase in cardiac tolerance to ischemia/reperfusion (I/R) is an urgent aim of physiology, pharmacology, and cardiac surgery, since I/R injury to the heart is often the cause of cardiogenic shock and subsequent death of patients in the postoperative period. We hypothesized that chronic continuous cold exposure can alter cardiac tolerance to I/R. Male Wistar rats were exposed to continuous cold exposure (+4°C, for 4 weeks). Rats which were subjected to coronary artery occlusion (45 min) and reperfusion (2 h) 24 h after cold adaptation. The selective cannabinoid 1 (CB1) receptor antagonist rimonabant, the selective CB2 receptor antagonist AM‐630, the transient receptor potential vanilloid channel (TRPV1) inhibitor capsazepine was administered intravenously 15 min before coronary artery occlusion. Chronic cold exposure enhanced tolerance to cold (–18 ○ C for 4 h), increased brown fat weight, adrenal weight, heart weight and serum triiodothyronine level but does not alter thymus, spleen weight, serum cortisol, corticosterone, and thyroxin levels. It was found that cold adaptation promoted a decrease in the infarct size/area at risk ratio by 33%. It was demonstrated that cannabinoid receptor antagonists did not eliminate the infarct‐reducing effect of cold adaptation. Capsazepine completely abolished the infarct‐limiting effect of cold adaptation. It was concluded that TRPV1 channel is involved in chronic cold‐induced cardiac tolerance to I/R.