Does regional hypothermia induced by coronary flow reduction affect refractoriness and conduction delay in open-chested dogs?
In open-chested dog models, changes in refractoriness and conduction during acute coronary flow reduction are significantly driven by regional temperature decreases rather than ischemia alone.
In the open-chested dog, coronary flow reduction results in a decrese of regional myocardial temperature (T). We assessed the contribution of T decrease to changes in refractoriness and conduction delay attributed to ischemia. The independent effect of regional hypothermia on effective refractory period (ERP) was a linear function of the temperature (ERP = -b T +a) with a -r = 0.97 0.02 in 11 dogs. The effect on conduction time of a ventricular premature beat was a linear function of the dog T at both endocardium (-r = 0.95 +/- 0.02) and epicardium (-r = 0.96 +/- 0.01). A 75% reduction in coronary flow resulted in a mean T decrease of 1.0 +/- 0.3 degrees C. The T decrease was sufficient to mask the effects of ischemia on shortening of the ERP. Furthermore, the conduction delay of ventricular premature beats during 75% coronary flow reduction could be accounted for by the decrease in T alone in five of seven dogs. We conclude that changes in refractoriness and conduction during acute coronary flow reduction in the open-chested dog are due to the composite effects of ischemia and the decrease in regional temperature. The open-chested model may have important limitations in understanding the electrophysiologic effects of acute coronary insufficiency. However, it may have important applications in defining the electrophysiologic environment at the time of coronary artery surgery.
Daniel et al. (Sun,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: