METABOLIC AND CARDIODYNAMIC RESPONSES OF ISOLATED TURTLE HEARTS TO ISCHEMIA AND REPERFUSION

We used P-31 and H-1 nuclear magnetic resonance spectroscopy to measure intracellular pH, high energy phosphates, and lactate levels in hearts of turtles (Chrysemys picta bellii) subjected to 1.5 h of global ischemia followed by reperfusion. We simultaneously monitored maximum ventricular developed pressure (P(max)), maximal rate of pressure development (dP/dt(max)), rate-pressure product (RPP), cardiac output, and heart rate and also measured lactate efflux from the hearts during reperfusion. Our goal was to test the hypothesis that turtle hearts would prove tolerant of prolonged global ischemia at 20-degrees-C and would recover completely on reperfusion without any indication of ischemia-or reperfusion-related injury. The 1.5 h of ischemia resulted in decreases in phosphocreatine and ATP to 31.4 +/- 2.8 and 87.3 +/- 6.3% of control, respectively, while P(i) rose to 236.6 +/- 26.3%. Intracellular pH decreased during this period from 7.38 +/- 0.02 to 6.87 +/- 0.04. Most of these changes occurred during the first 30 min. Tissue lactate rose during 1.5 h of ischemia from almost-equal-to 1.5 to 22.3-mu-mol/g wet tissue wt. However, the rate of lactate production was much higher during the first 21 min of ischemia (0.41-mu-mol.g-1.min-1) than during the remaining 70 min (0.10-mu-mol.g-1.min-1). With the onset of ischemia, P(max), dP/dt(max), RPP, and heart rate all decreased dramatically with roughly the same time course as the changes in high-energy phosphates and intracellular pH. On reperfusion, turtle hearts rapidly restored high-energy phosphates, intracellular pH, lactate, and cardiodynamics to control levels, usually within 15-30 min, with no evidence of reperfusion injury. Our data support the hypothesis that turtle hearts rapidly decrease their anaerobic metabolic rates during ischemia and can then survive for prolonged periods of time in this new metabolically depressed steady state. In contrast to ischemic mammalian myocardium, ATP is conserved, acidosis develops slowly, and full recovery occurs rapidly upon reperfusion.