Resistance to myocardial infarction induced by heat stress and the effect of ATP-sensitive potassium channel blockade in the rat isolated heart

Abstract

1. Heat stress (HS) is known to protect against myocardial ischaemia-reperfusion injury by improving mechanical dysfunction and decreasing necrosis. However, the mechanisms responsible for this form of cardioprotection remain to be elucidated. ATP-sensitive potassium (K(ATP)) channels have been shown to be involved in the delayed phase of protection following ischaemic preconditioning, a phenomenon closely resembling the HS-induced cardioprotection. The aim of this study was thus to investigate the role of K(ATP) channels in HS-induced protection of the isolated rat heart. 2. Twenty four hours after whole body heat stress (at 42°C for 15 min) or sham anaesthesia, isolated perfused hearts were subjected to a 15 min stabilization period followed by a 15 min infusion of either 10 μM glibenclamide (Glib), 100 μM sodium 5-hydroxydecanoate (5HD) or vehicle (0.04% DMSO). Regional ischaemia (35 min) and reperfusion (120 min) were then performed. 3. Prior heat stress significantly reduced infarct-to-risk ratio (from 42.4 ± 2.4% to 19.4 ± 2.9 P < 0.001). This resistance to myocardial infarction was abolished in both Glib-treated (40.1 ± 1.8% vs 42.3 ± 1.8%) and 5HD-treated (41.2 ± 1.8% vs 41.8 ± 1.2%) groups. 4. The results of this study suggest that K(ATP) channel activation contributes to the cytoprotective response induced by heat stress.