The inotropic consequences of cooling: studies in the isolated rat heart.

To investigate the controversial effects of hypothermia on cardiac contractile performance, we have carried out ventricular volume-loading experiments in 23 perfused, paced (2 Hz), isolated rat hearts, contracting isovolumically at various temperatures. A water-filled, unstressed latex balloon was inserted into the left ventricle and its volume was controlled with a microsyringe. Left ventricular pressure (LVP), its first derivative (dP/dt) and coronary flow were recorded. One group of hearts (n = 7) were perfused at 37 degrees C over 2 h. Another group of hearts (n = 16) were cooled in a stepwise manner from 37 degrees C to 21 degrees C, with 10-min perfusion at each of seven different temperatures, and then rewarmed to 37 degrees C. Emax, an index of contractility, calculated as the slope of the regression line of the end-systolic pressure-volume relationship, was found to increase as temperature fell (3.9, 4.6, 4.9, 5.5, 5.5, 6.2, and 6.3 cm H2O/microliters at 37 degrees, 34 degrees, 31 degrees, 29 degrees, 27 degrees, 24 degrees and 21 degrees C, respectively) while it remained constant over the 2-h perfusion in the normothermic perfusion group. By contrast, peak positive dP/dt/peak-developed pressure (+dP/dt/DP) progressively decreased during cooling without any change in the normothermic perfusion group. The results indicate that hypothermia can be designated as a positive inotropic intervention in terms of force-generation (Emax) but as a negative inotropic intervention in terms of shortening velocity of contractile element in Hill's model (+dP/dt/DP).