Effect of temperature on myocardial infarction in swine

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 degrees 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 (r(2) = 0.71, P = 0.0001) so that at 35 degrees C no infarction occurred and with each 1 degrees 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.