Impairment of cardiopulmonary baroreflex after cardiac transplantation in humans

Abstract

There is ample evidence for efferent cardiac denervation in patients after cardiac transplantation. However, little is known regarding the effects of the cardiac deafferentation that also results. We examined responses to graded lower-body negative pressure and thus cardiopulmonary baroreceptor unloading in 23 patients 3 to 12 months after cardiac transplantation and compared their responses with those of nine normal subjects. Responses of mean arterial pressure, forearm vascular resistance, and plasma norepinephrine were assessed during lower-body negative pressure and the cold pressor test. Reflex increases in forearm vascular resistance (1.5 ± 1, 5.0 ± 1.4, and 6.4 ± 2.1 vs 14.5 ± 4.5, 20.3 ± 6.5, and 34 ± 11 units) and plasma norepinephrine (42 ± 12, 58 ± 15, and 62 13 vs 49 ± 14, 94 ± 25, and 173 ± 36 pg/ml) during lower-body negative pressure (at -10, -20, and -40 mm Hg) were strikingly smaller in cardiac transplant patients than in normal subjects. The impaired responses of the cardiac transplant patients were not the result of a nonspecific depression of cardiovascular reflexes, since increases in mean arterial pressure (12 ± 3 vs 10 ± 2 mm Hg), forearm vascular resistance (19.5 ± 3.4 vs 18 ± 5.8 units), and plasma norepinephrine (56 ± 8 vs 42 ± 11 pg/ml) during cold pressor test were not significantly different in the two groups. Furthermore, the impaired responses were not caused by the immunosuppressive agents used to treat the cardiac transplant patients, since patients with renal transplants on similar regimens had augmented forearm vasoconstrictor responses. The technique of orthotopic transplantation we used results mainly in ventricular deafferentation. Thus our data suggests that cardiopulmonary baroreflex control of forearm vascular resistance is impaired after cardiac transplantatation and that this is due mainly to ventricular deafferentation.