To study the responses of myocardial function and metabolism to
hypoxia in normal hamsters and cardiomyopathic hamsters (Bio 14.6), left ventricular pressure was measured in an isolated isovolumically beating heart preparation, and myocardial high energy
phosphates (
ATP and
creatine phosphate),
inorganic phosphate, and intracellular pH were also measured by 31P nuclear magnetic resonance spectroscopy. In 20-week-old cardiomyopathic hamsters, the heart weight was increased and the baseline left ventricular developed pressure, peak positive dP/dt, and peak negative dP/dt were decreased, indicating depression of left ventricular function. In control hamsters, left ventricular end-diastolic pressure rose markedly (+481 +/- 70%), and left ventricular developed pressure decreased (-57 +/- 6%) during 30 mins period of hypoxic perfusion. Correspondingly, myocardial content of
ATP (-42 +/- 17%) and
creatine phosphate (-48 +/- 14%) was decreased and that of
inorganic phosphate was increased (+185 +/- 127%). Intracellular pH was also decreased (-0.20 +/- 0.13). In contrast, cardiomyopathic hamsters, showed a relatively slight increase in left ventricular end-diastolic pressure (+106 +/- 83%, P < 0.01 vs. control hamsters), although the decrease in left ventricular developed pressure (-50 +/- 5%) was comparable to that in control hamsters. The recovery of left ventricular end-diastolic pressure and developed pressure during reoxygenation was better in cardiomyopathic hamsters. The decrease in myocardial
ATP (-13 +/- 26%, P < 0.01 vs. control hamsters), the increase in
inorganic phosphate (+95 +/- 88%, P < 0.05 vs. control hamsters), and the decrease in intracellular pH (-0.06 +/- 0.06, P < 0.01 vs. control hamsters) during
hypoxia were much less marked in cardiomyopathic hamsters. Only the decrease in
creatine phosphate (-32 +/- 16%) was comparable to that in control hamsters. Thus, in cardiomyopathic hamsters, the deterioration of left ventricular diastolic function, systolic function, and myocardial energy metabolism during
hypoxia was mild compared with the change in control healthy hamsters. This increased tolerance of cardiomyopathic hearts to
hypoxia may be related to alterations in myocardial
contractile proteins and/or energy utilization, or substrate availability.