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Functional, metabolic and structural studies of the chronic canine cardiac autotransplant

1972; Elsevier BV; Volume: 13; Issue: 6 Linguagem: Inglês

10.1016/0022-4804(72)90077-7

1095-8673

E. A. Shanahan, Willard M. Daggett, Lee V. Leak, Joseph B. Warshaw, Edward Lowenstein, Richard R. Lower, William G. Austen,

Mechanical Circulatory Support Devices

To assess the degree and time course of cholinergic autonomic reinnervation, five dogs, 13 months to 5 years after cardiac autotransplantation, were studied in a controlled hemodynamic setting. Myocardium of these autotransplanted hearts was submitted to electron microscopy to detect any structural changes present. Mitochondrial yield and energy yielding reactions were assessed to clarify the possibility of an altered state of myocardial metabolism. With cardiac output and aortic pressure held constant, vagal nerve stimulation caused bradycardia in all five animals. With heart rate held constant by atrioventricular pacing, vagal stimulation caused depression of left ventricular performance in four of the five dogs. These effects were abolished by intravenously administered atropine. Mitochondrial yields from normal and autotransplanted myocardium were identical. Oxidative phosphorylation of NADH linked substrates, fatty acid oxidation, and direct assay of palmitylcarnitine transferase did not differ in autotransplanted versus normal myocardium. Ultrastructure did not differ significantly in autotransplanted versus normal myocardium. Sympathetic reinnervation of the autotransplanted canine heart has been previously documented; however, cholinergic reinnervation of the left ventricle has herein been demonstrated for the first time. Data on mitochondrial metabolism and myocardial ultrastructure support the position that extrinsic cardiac denervation is not attended by significant long-term metabolic or morphologic alterations of the autotransplanted myocardium.