Heat stress attenuates free radical release in the isolated perfused rat heart

Prior heat stress leads to an enhancement of postischemic mechanical function and improvement in biochemical indices of injury in the rat heart, associated with an elevation in endogenous catalase activity. We have examined the effect of heat stress on free radical release during reperfusion in the...

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Veröffentlicht in:Free radical biology & medicine 1993-10, Vol.15 (4), p.459-463
Hauptverfasser: Mocanu, Mihaela M., Steare, Stephen E., Evans, Michael C.W., Nugent, Jonathan H., Yellon, Derek M.
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container_end_page 463
container_issue 4
container_start_page 459
container_title Free radical biology & medicine
container_volume 15
creator Mocanu, Mihaela M.
Steare, Stephen E.
Evans, Michael C.W.
Nugent, Jonathan H.
Yellon, Derek M.
description Prior heat stress leads to an enhancement of postischemic mechanical function and improvement in biochemical indices of injury in the rat heart, associated with an elevation in endogenous catalase activity. We have examined the effect of heat stress on free radical release during reperfusion in the isolated rat heart using electron spin resonance (ESR). Twenty four hours after heat stress or sham treatment, hearts were perfused in the Langendorff mode and subjected to 10 min of no-flow global ischemia followed by 10 min of reperfusion. Coronary effluent was collected at specific time points in PBN for ESR measurement. A PBN adduct was identified with characteristics consistent with an alkoxyl radical: PBN-LO. In sham hearts there was a rapid rise in adduct release to a maximuum (228 ± 15% of stabilization values, p < .05) occurring 1 min into reperfusion. In heat stress hearts there was no significant rise in adduct release during the reperfusion period. Pretreatment of hearts with 3-amino triazole, an inhibitor of catalase, failed to clarify whether the protection seen in heat stress hearts was a result of the elevation in catalase activity. These results suggest that heat stress protects the myocardium against the oxidative stress of ischemia-reperfusion.
doi_str_mv 10.1016/0891-5849(93)90046-W
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We have examined the effect of heat stress on free radical release during reperfusion in the isolated rat heart using electron spin resonance (ESR). Twenty four hours after heat stress or sham treatment, hearts were perfused in the Langendorff mode and subjected to 10 min of no-flow global ischemia followed by 10 min of reperfusion. Coronary effluent was collected at specific time points in PBN for ESR measurement. A PBN adduct was identified with characteristics consistent with an alkoxyl radical: PBN-LO. In sham hearts there was a rapid rise in adduct release to a maximuum (228 ± 15% of stabilization values, p &lt; .05) occurring 1 min into reperfusion. In heat stress hearts there was no significant rise in adduct release during the reperfusion period. Pretreatment of hearts with 3-amino triazole, an inhibitor of catalase, failed to clarify whether the protection seen in heat stress hearts was a result of the elevation in catalase activity. 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subjects Alkoxyl free radical
Animals
Biological and medical sciences
Catalase
Electron spin resonance
Electron Spin Resonance Spectroscopy
Free Radicals
Fundamental and applied biological sciences. Psychology
Global ischemia
Heart
Heat stress
Hemodynamics
Hot Temperature
Male
Myocardial Ischemia
Myocardial Reperfusion
Myocardium - metabolism
PBN
Perfusion
Rats
Rats, Sprague-Dawley
Reperfusion
Vertebrates: cardiovascular system
title Heat stress attenuates free radical release in the isolated perfused rat heart
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