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 degrees 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 microM glibenclamide (Glib), 100 microM 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.
journal_name
Br J Pharmacoljournal_title
British journal of pharmacologyauthors
Joyeux M,Godin-Ribuot D,Ribuot Cdoi
10.1038/sj.bjp.0701710subject
Has Abstractpub_date
1998-03-01 00:00:00pages
1085-8issue
6eissn
0007-1188issn
1476-5381journal_volume
123pub_type
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