Background: High cardiac workloads produced by catecholamine infusion resul
t in loss of myocardial phosphocreatine (PCr) and accumulation of inorganic
phosphate (Pi) which are more prominent in hearts with left ventricular hy
pertrophy (LVH) than in normal hearts. Since ischemia can cause changes in
phosphorylated compounds similar to those during catecholamine stimulation,
this study tested the hypothesis that the exaggerated depletion of PCr and
accumulation of Pi during high workloads in LVH is the result of impaired
myocyte oxygenation. Methods and results: P-31- and H-1-NMR spectroscopy we
re used to determine myocardial high energy phosphate levels and myoglobin
desaturation, respectively, in eight normal dogs and nine dogs with LVH pro
duced by ascending aortic banding. The mean LV weight/body weight ratio was
approximately twice normal in the LVH group. Infusion of dobutamine (15 an
d 30 mu g/kg/min), and dobutamine+dopamine (each 20 mu g/kg/min) caused pro
gressive similar increases in the heart rateXsystolic LV pressure product t
o a maximum of 57.4+/-3.3.10(3) in normal and 63.9+/-2.7.10(3) in LVH anima
ls, while myocardial oxygen consumption increased from 0.09+/-0.01 to 0.24/-0.04 in normals and from 0.10+/-0.02 to 0.25+/-0.03 ml/min/g in LVH. PCr/
ATP ratios during basal conditions were lower in LVH hearts (1.73+/-0.10, 1
.61+/-0.09 and 1.51+/-0.09 in subepicardium, midwall and subendocardium, re
spectively) as compared with normals (2.24+/-0.09, 2.01+/-0.08 and 1.89+/-0
.07; each p<0.01 normal vs. LVH). Catecholamine infusions caused dose-relat
ed decreases in PCr/ATP and appearance of Pi which was more marked in LVH t
han in normal hearts. H-1-NMR spectroscopy did not detect deoxymyoglobin in
either normal or LVH hearts even during the highest workloads. In contrast
, occlusion of the anterior descending coronary artery resulted in a large
deoxymyoglobin signal. Conclusions: Increases of cardiac work produced by c
atecholamine stimulation resulted in greater decreases of PCr and greater i
ncreases of Pi in hypertrophied than in normal hearts. These abnormalities
were not the result of inadequate intracellular oxygen availability and con
sequently cannot be ascribed to demand ischemia. (C) 1999 Elsevier Science
B.V. All rights reserved.