The effect of ischemic arrest (IA) on ventricular relaxation and the diastolic pressure-volume (P/V) relationship was studied in 17 isolated, perfused, isovolumic feline hearts. During one hour of IA, nine hearts were maintained at normothermia (NIA) and eight were cooled to 27°C hypothermia (HIA). Maximum dP/dt was used as an index of contractility. P/V curves were inscribed by constant volume infusion into an intraventricular balloon and plotted according to the equation Pd = βe (dVd), where Pd = end diastolic pressure; Vd = end diastolic volume; (stiffnes constant) = slope of in Pvs Vd; and β = InP intercept at Vd = 0. To normalize for initial cavity size, curves were replotted as Pd vs (Vd-Vo)/V0, where Vo = volume at Pd of 10 mm Hg. Left ventricular relaxation was assessed by changes in the time constant (T) of isovolumic pressure fall after max-dP/dt (T = -1/A, where p = e - At + D). Results after one hour of IA and 30 min. of reperfusion are given in a table as mean ± SEM. Prolongation of the relaxation phase of the cardiac cycle accompanied impaired contractility in the post arrest heart and hypothermia provided significant protection to the active relaxing system. These data also suggest that the mechanism of an elevation of Pd in isovolumic hearts following IA is not increased ventricular stiffness, but a reduction in left ventricular diastolic volume at constant and diastolic pressure.
|Original language||English (US)|
|State||Published - 1977|
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