Abstract
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 (KATP) 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 KATP channels in HS-induced protection of the isolated rat heart.
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.
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.
The results of this study suggest that KATP channel activation contributes to the cytoprotective response induced by heat stress.
Keywords: Heat stress, infarct size, KATP channel, glibenclamide, sodium 5-hydroxydecanoate
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