Differential Characteristics of Neural Circulatory Control

Abstract

Background-Reappearance of low-frequency (LF) (Ϯ0.10 Hz) oscillations in RR interval (RR) after cardiac transplantation is indicative of sympathetic efferent reinnervation. We hypothesized that restored LF oscillations in RR in heart transplant recipients (HTRs) are linked to oscillations in muscle sympathetic nerve traffic (MSNA). Methods and Results-RR, RR variability, and MSNA were recorded 5Ϯ2 months (nϭ7, short-term HTRs) and 138Ϯ8 months (nϭ7, long-term HTRs) after heart transplantation and compared with matched hypertensive patients (nϭ7). A coherence function determined the coupling between LF oscillations in MSNA and RR. RR variance did not differ between short-term and long-term HTRs. However, LF variability was only 1Ϯ0.5 ms 2 in the short-term HTRs but was 15Ϯ8 ms 2 in the long-term HTRs (PϽ0.05). Normalized LF variability was also higher in the long-term HTRs (40Ϯ14 normalized unites) versus the short-term HTRs (6Ϯ3 normalized united, PϽ0.05) but did not differ from the LF variability of the hypertensive patients. Long-term HTRs were taking less cyclosporine (PϽ0.01) but had higher MSNA than the short-term HTRs (62Ϯ7 versus 31Ϯ7 burst/min, respectively, PϽ0.05). Coherence between LF oscillations in MSNA and RR was similar in the long-term HTRs (0.59Ϯ0.11) and the hypertensive patients (0.60Ϯ0.07) and was 3-fold greater than in the short-term HTRs (0.20Ϯ0.06, PϽ0.05). Conclusions-Cardiac reinnervation after long-term heart transplantation is characterized by a restoration of the coherence between LF oscillations in RR and MSNA. Higher MSNA in long-term than in short-term HTRs suggests that time elapsed after cardiac transplantation may be a major determinant of sympathetic excitation in heart transplant recipients.

Effects of Peripheral Chemoreceptors Deactivation on Sympathetic Activity in Heart Transplant Recipients

“…These studies revealed that cyclosporine and time from heart transplantation contribute to MSNA increase in HTRs. 2,3 Our study confirms previous observations of increased MSNA in long-term HTRs. It provides a new insight into sympathetic regulation after heart transplantation.…”

“…Heart transplantation initially decreases the MSNA related to the heart failure state, because it returns to normal values within 1 year after the surgical procedure, 16 although this normalization does not seem to be permanent. 2,3 Only a few studies have used direct recording of nerve traffic to unravel sympathetic activation after heart transplantation. These studies revealed that cyclosporine and time from heart transplantation contribute to MSNA increase in HTRs.…”

“…1 Heart transplantation restores a close to normal cardiac function but does not always normalize MSNA. [2][3][4][5] Elevated MSNA after heart transplantation is associated with cyclosporine therapy 3 and increases as a function of time after transplantation. 2 Increased peripheral chemoreflex sensitivity has been demonstrated in humans and experimental animals with congestive heart failure.…”

“…[2][3][4][5] Elevated MSNA after heart transplantation is associated with cyclosporine therapy 3 and increases as a function of time after transplantation. 2 Increased peripheral chemoreflex sensitivity has been demonstrated in humans and experimental animals with congestive heart failure. 6 -9 Whether this alteration in chemoreflex function is reversible when cardiac function is restored by heart transplantation is unknown.…”

Decreased heart rate and blood pressure in a recent cardiac transplant patient after spinal anesthesia

“…Afferent reinnervation is supported by reports of angina accompanied by objective evidence of cardiac ischemia. 9,10 Evidence for sympathetic reinnervation derives from the emergence of a low-frequency heart rate (HR) variability in some transplants, [11][12][13] and the appearance of appropriate, albeit diminished, reflex changes in HR. 11,[14][15][16] In addition, experiments suggest catecholamine uptake, storage or release from presumed cardiac sympathetic postganglionic neurons in the transplanted heart.…”