Dj. Duncker et al., EFFECT OF TEMPERATURE ON MYOCARDIAL-INFARCTION IN SWINE, American journal of physiology. Heart and circulatory physiology, 39(4), 1996, pp. 1189-1199
Body core temperature in the normothermic range alters infarct size in
rabbits. Moreover, temperature may modulate the protection by adenosi
ne during a coronary artery occlusion. We investigated the effect of c
ore temperature within the normothermic range (35-39 degrees C) on myo
cardial infarct size produced by a 45-min coronary occlusion in open-c
hest swine (n = 10), and we determined whether adenosine blockade with
8-phenyltheophylline and adenosine deaminase increased infarct size i
n the normothermic range (n = 9). After 4 h of reperfusion the area at
risk and infarct size were determined with Evans blue dye and triphen
yltetrazolium chloride. Infarct size strongly correlated with temperat
ure (r(2) = 0.71, P = 0.0001) so that at 35 degrees C no infarction oc
curred and with each 1 degrees C increase in temperature 20% of the ar
ea at risk became infarcted. In contrast, neither the low levels of co
llateral flow (0.03 +/- 0.01 ml . min(-1) . g(-1)) nor the rate-pressu
re product correlated with infarct size. In the normothermic range, ad
enosine blockade had no effect on infarct size. The data demonstrate t
hat temperature can exert a profound effect on infarct size but fail t
o demonstrate a protective effect of endogenous adenosine at normother
mic temperatures. Our findings emphasize the need for stringent contro
l of core temperature during investigation of interventions aimed at r
educing infarct size.