Effect of temperature on myocardial infarction in swine

Dirk J. Duncker, Christopher L. Klassen, Yutaka Ishibashi, Sara H. Herrlinger, Todd J. Pavek, Robert J. Bache

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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 languageEnglish (US)
Pages (from-to)H1189-H1199
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4 39-4
StatePublished - 1996


  • coronary artery occlusion
  • ischemia
  • myocardial blood flow
  • myocardial oxygen demand
  • reperfusion
  • systolic wall thickening


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