Abstract
Body core temperature in the normothermic range alters infarct size in rabbits. Moreover, temperature may modulate the protection by adenosine during a coronary artery occlusion. We investigated the effect of core temperature within the normothermic range (35-39°C) on myocardial infarct size produced by a 45-min coronary occlusion in open-chest swine (n = 10), and we determined whether adenosine blockade with 8-phenyltheophylline and adenosine deaminase increased infarct size in the normothermic range (n = 9). After 4 h of reperfusion the area at risk and infarct size were determined with Evans blue dye and triphenyltetrazolium chloride. Infarct size strongly correlated with temperature (r2 = 0.71, P = 0.0001) so that at 35°C no infarction occurred and with each 1°C increase in temperature 20% of the area at risk became infarcted. In contrast, neither the low levels of collateral flow (0.03 ± 0.01 ml · min-1 · g-1) nor the rate-pressure product correlated with infarct size. In the normothermic range, adenosine blockade had no effect on infarct size. The data demonstrate that temperature can exert a profound effect on infarct size but fail to demonstrate a protective effect of endogenous adenosine at normothermic temperatures. Our findings emphasize the need for stringent control of core temperature during investigation of interventions aimed at reducing infarct size.
Original language | English (US) |
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Pages (from-to) | H1189-H1199 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 270 |
Issue number | 4 39-4 |
DOIs | |
State | Published - 1996 |
Keywords
- coronary artery occlusion
- ischemia
- myocardial blood flow
- myocardial oxygen demand
- reperfusion
- systolic wall thickening