Epicardial temperature is a major predictor of myocardial infarct size in dogs.

To determine whether epicardial temperature varies among anesthetised, open-chest dogs, and, if so, whether such variation has a measurable effect on myocardial infarct size, 35 open-chest mongrel dogs underwent 60 min of circumflex coronary artery occlusion and 3 h of reperfusion. Infarct size was measured using triphenyl tetrazolium chloride (TTC) macrochemistry. Known predictors of infarct size including area-at-risk (AAR) and collateral blood flow (CBF) were measured. Epicardial temperature was monitored using a temperature probe placed in the pericardial space adjacent to the posterior surface of the heart. In each individual dog, epicardial temperature was nearly constant throughout the period of coronary occlusion. Amongst dogs, however, epicardial temperature ranged from 35.5-41.0 degrees C. By multiple regression analysis, infarct size was better predicted by the combination of temperature and CBF than by CBF alone. "Low-T" (35.5-38.0 degrees C, n = 17) and "high-T" (38.1-41.0 degrees C, n = 18) subgroups were compared by analysis of covariance (ANCOVA), using infarct size as the dependent variable and CBF as the independent variable. Following adjustment of infarct size for CBF, infarct size in the low-T subgroup was only 53% v that in the high-T subgroup (16.9 +/- 2.7% v 31.9 +/-5.0% of AAR, P < 0.001). Thus, in open-chest dogs, relatively minor variation in epicardial temperature had major effects on myocardial infarct size. We conclude that myocardial temperature is an independent predictor of infarct size in dogs. Although such variation could confound studies of the therapeutic efficacy of proposed cardioprotective interventions, controlling for temperature variation in such studies should reduce the likelihood of false positive or negative results.

Intracoronary administration of the alpha 1-receptor agonist, methoxamine, does not reproduce the infarct-limiting effect of ischemic preconditioning in dogs.

BACKGROUND: The cardioprotective effect of ischemic preconditioning has been hypothesized to occur through one or more signalling mechanisms which activate protein kinase C. Stimulation of alpha 1-adrenergic receptors by catecholamines released during the preconditioning episodes of ischemia is one of these putative signalling mechanisms. METHODS: To determine whether stimulation of alpha 1-adrenergic receptors before an ischemic challenge can mimic preconditioning, anesthetized dogs were treated with 4 intracoronary infusions of methoxamine HCl (10 micrograms/kg/min; n = 8), each 5 min in duration and followed by 5 min of washout. Control dogs (n = 10) were given similar infusions of 0.9% NaCl. A third group of dogs was preconditioned with 4 cycles of 5 min ischemia, each followed by 5 min of reperfusion (n = 8). All dogs then underwent 60 min of ischemia (circumflex coronary occlusion) followed by 3 h of reperfusion. Infarct size (expressed as % of area-at-risk) was measured with TTC macrochemistery and analyzed (using analysis of covariance [ANCOVA]) with respect to coronary collateral blood flow (measured using radioactive microspheres). RESULTS: Methoxamine markedly increased systemic arterial and left atrial pressures prior to but not during the ischemic challenge. Baseline predictors of infarct size were not different among the groups. Mean infarct size (adjusted from ANCOVA) did not differ between control and methoxamine-treated groups, 28.3 +/- 2.8% vs. 29.7 +/- 3.2%, respectively (P = NS), but was only 12.7 +/- 3.2% in the preconditioned group (P < 0.01 vs. control and methoxamine). CONCLUSIONS: A series of methoxamine infusions before an ischemic challenge did not affect infarct size. Thus, stimulation of alpha 1-adrenergic receptors alone is insufficient to mimic the cardioprotective effect of ischemic preconditioning in this canine model.