Abstract
ObjectivePrevious experimental studies have demonstrated that mild reductions in body temperature can decrease infarct size in the setting of acute myocardial infarction (MI). However, it has been suggested that the cardioprotective effects of mild hypothermia and other conditioning interventions are attenuated by concomitant administration of propofol. To address this issue, we evaluated the relationship between body temperature and infarct size in propofol‐anesthetized swine subjected to prolonged myocardial ischemia and reperfusion.MethodsSwine (n=17) were anesthetized with propofol (10 mg/kg/hour) and subjected to a 60‐minute balloon occlusion of the distal left anterior descending coronary artery (LAD) in the closed‐chest state. Serum cTnI values were quantified by a porcine‐specific ELISA at baseline and 1‐hour after reperfusion. Infarct size (triphenyl tetrazolium chloride) and ischemic area‐at‐risk (AAR; phthalocyanine blue during coronary re‐occlusion) were assessed post‐mortem 3‐hours (n=2), 24 hours (n=5), or 7 days (n=10) after reperfusion.ResultsDirect, statistically significant (p<0.01) correlations were observed between body temperature at reperfusion and infarct size relative to AAR (r=0.75), infarct size relative to LV mass (r=0.70), and serum cTnI 1‐hour after reperfusion (r=0.78). When animals were divided into two groups based on median body temperature at reperfusion (37.5 °C), animals with a body temperature <37.5 °C exhibited significantly smaller infarcts and lower serum cTnI values than animals with a body temperature > 37.5 °C (Table). Importantly, low body temperature‐related reductions in infarct size were observed in the absence of group differences in the duration of reperfusion, LV mass, and ischemic AAR.ConclusionThese results demonstrate that the cardioprotective effect of mild hypothermia is not attenuated in the setting of propofol anesthesia. Furthermore, the marked reduction in infarct size associated with relatively minor diminutions in body temperature provides further support for the notion that even modest reductions in body temperature within a normothermic range may be an effective approach to limit infarct size in patients with acute MI.Support or Funding InformationThe National Heart Lung and Blood Institute (HL‐061610), the American Heart Association (17SDG33660200), the National Center for Advancing Translational Sciences (UL1TR001412), the Department of Veterans Affairs (1IO1BX002659), the New York State Department of Health (NYSTEM CO24351, the UB Center for Undergraduate Research and Creative Activities, and the Albert and Elizabeth Rekate Fund in Cardiovascular Medicine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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