Work Capacity and Efficiency of the Autotransplanted Heart
Total extrinsic denervation of the heart was accomplished in six animals by cardiac autotransplantation. The work capacity and efficiency were studied in the postoperative period, when there was depletion of catecholamine stores. The left ventricular oxygen consumption (VO2) of these six cardiac autotransplants (average body weight, 13.6±0.6 kg) and six normal dogs (average body weight, 14.0±0.4 kg) were compared with a right-heart bypass at similar heart rates, mean arterial blood pressures, and systemic flows. The two groups of animals achieved comparable levels of stroke work (17.3 g-m) over the same range of filling pressures. Average maximum rates of left ventricular pressure development were also similar (autotransplants 2455±278 mm Hg/sec, versus 2267±209 mm Hg/sec for normal dogs). At VO2/100 g left ventricle, autotransplants averaged 9.54±0.97 cc/min and normal dogs 9.62±0.76 cc/min. However, left ventricular weights in the autotransplant group were significantly greater (110.9±6.2 g) than in the normal dogs (96.7±3.4 g), and represented a significantly greater percentage of body weight (8.2±0.5% versus sus 6.6±0.3%). Total left ventricular VO2 was greater in autotransplants during performance of comparable levels of external work and at comparable degrees of contractility. No systematic difference in handling of glucose, lactate, or pyruvate was noted between the groups. Respiratory quotients were 1.0 or greater. The normal dogs showed no net change in circulating catecholamines across the coronary bed, whereas autotransplants always showed a net uptake of catecholamines. Myocardial mitochondria were enlarged in electron micrographs of the ventricular myocardium of the autotransplants.
The totally extrinsically denervated cardiac autotransplant can achieve a level of performance similar to that of a normal heart, but is less efficient in doing so. Alterations in utilization of circulating catecholamines may aid the hemodynamic adaptation to the cardiac denervation.
- © 1967 American Heart Association, Inc.