Myocardial oxygen consumption during experimental hypertrophy and congestive heart failure

Abstract

The purpose of this investigation was to study the effects of experimental myocardial hypertrophy-congestive failure state on myocardial oxygen consumption (MV̇O 2). Hypertrophy and heart failure were induced in nine adult cats by surgical banding of the main pulmonary artery to a lumen approximately 10% of normal (2.8 mm circumference clip). Twenty-five to 82 days later nine CHF and 12 control animals were studied, and right ventricular papillary muscles were mounted in a polarographic oxygen electrode muscle bath for simultaneous determination of myocardial mechanics and MV̇O 2. Pulmonary arterial banding resulted in average peak systolic right ventricular pressure of 73 ± 7 mmHg and right ventricular/body weight ratio was increased from 0.54 ± 0.08 control to 1.22 ± 0.08 g/kg CHF ( P < 0.001). Right ventricular end-diastolic pressure was increased from 1.9 ± 0.2 control to 9.0 ± 1.1 mmHg CHF ( P < 0.001) while liver weight/body weight ratio was increased from 27.8 ± 1.1 control to 31.7 ± 1.5 g/kg CHF ( P < 0.01). The average force velocity curve was depressed downward and to the left with maximal measured velocity (preload) changing from 1.35 ± 0.07 control to 0.62 ± 0.06 muscle lengths/s ( P < 0.001). The extent of shortening and thus the external work performed was significantly depressed in CHF muscles. However, MV̇O 2 of afterload contractions of CHF muscles was entirely normal. The length-active tension relationship was significantly depressed with peak developed tension at L max in CHF muscles of 3.55 ± 0.53 g/mm 2 (control 6.19 ± 0.55, P < 0.01). Although the rate of tension development of isometric contractions was depressed from 34.1 ± 3.3 control to 14.7 ± 0.19 g/mm 2/s CHF ( P < 0.001), the MV̇O 2 per gram of tension development was paradoxically increased from 0.56 to 1.17 μl/mg/contraction × 10 −3. Resting MV̇O 2 was increased from 2.07 ± 0.19 control to 4.27 ± 0.53 μl/mg/h. The effect of acetylstrophanthidin 2 × 10 −7 g/ml was to increase both the contractile state and MV̇O 2 of CHF muscles. These findings demonstrate an inefficiency of conversion of oxygen to tension development in experimental hypertrophy and congestive heart failure.