Acute hibernation and reperfusion of the ischemic heart

Recovery from prolonged low-flow ischemia was studied in isolated, isovolumically beating neonatal piglet hearts (n = 11) and compared with controls (n = 5).

Hearts were perfused with red blood cell-enhanced Krebs-Henseleit buffer with physiological oxygen-carrying capacity. Left ventricular mechanical function was assessed with a fluid-filled balloon. Measurements of peak systolic pressure, pressure-rate product (PRP), and +dP/dtmax were obtained at various filling pressures. Myocardial oxygen delivery and metabolism (MVO2) and lactate uptake were measured at 30-minute intervals. Control data were obtained with coronary flow (CF) set at 2 ml.min-1.g-1. CF was then reduced to 0.2 ml.min-1.g-1 for 2 hours. Thereafter, reperfusion was instituted at control levels. Hearts not subjected to ischemia were studied at identical time intervals. In these, function remained at greater than 80% after more than 3.5 hours of study. Reduction of CF to 10% was accompanied by an abrupt diminution in function (pressure-rate product) and MVO2 to 20% of control and by lactate release. These measures remained constant for the full 2 hours of ischemia. Incremental return of CF caused a lockstep increase in mechanical function and metabolism. At 30 minutes of reperfusion, PRP was 78% of time-matched controls (p = 0.05), and dP/dtmax did not differ. Increasing calcium to 5 mmol/l returned PRP (and dP/dtmax) to preischemia levels. Myocardial ATP and creatine phosphate concentrations were identical in both groups, although glycogen was lower in the ischemic hearts.

Acute hibernation is associated with protection of the in vitro heart from prolonged normothermic ischemia. Systolic function was only modestly lower, and velocity (dP/dtmax) did not differ from control hearts. The minimal "stunning" was fully reversible with calcium.