The present study was undertaken to define the effects of
left ventricular hypertrophy on postischemic recovery of myocardial performance and high energy
phosphate metabolism. Hemodynamics and 31P-magnetic resonance spectra were monitored simultaneously in the isolated Langendorff-perfused rat heart during 30 minutes of
ischemia and 30 minutes of reperfusion.
Left ventricular hypertrophy was produced by either suprarenal aortic constriction or chronic
thyroxine administration. In chronic pressure overload
hypertrophy, minimal coronary resistance was significantly higher (p less than 0.001) and the loss of
purine nucleosides in the coronary effluent during early reperfusion significantly larger (p less than 0.001) compared with both normal hearts and
thyroxine-induced hypertrophied hearts. Postischemic recovery of the baseline values for left ventricular developed pressure and phosphorylation potential was 43 +/- 4% and 82 +/- 4%, respectively, in chronic pressure overload hypertrophied hearts; 86 +/- 4% and 91 +/- 3%, respectively, in normal hearts (chronic pressure overload
hypertrophy versus normal hearts, p less than 0.001 and p less than 0.05); and 100 +/- 4% and 98 +/- 2%, respectively, in
thyroxine-induced hypertrophied hearts (normal hearts versus
thyroxine-induced hypertrophied hearts, p less than 0.05 and p less than 0.05). Recovery after reperfusion was not related to intracellular pH,
ATP,
phosphocreatine, or
inorganic phosphate levels during
ischemia. Also, recovery was not related to developed pressure or oxygen consumption before
ischemia. However, recovery was inversely related to coronary resistance and directly related to coronary flow before
ischemia. Thus, functional and/or anatomic alterations of the coronary vascular bed and a greater loss of
purine nucleosides during reperfusion are likely responsible for the attenuated compensatory response to
ischemia and reperfusion in
left ventricular hypertrophy induced by chronic pressure overload. On the other hand, the excess muscle mass per se does not seem to alter recovery, since
thyroxine-induced myocardial hypertrophied hearts responded at least as well as normal hearts.