RESPIRATORY SINUS DYSRHYTHMIA PERSISTS IN TRANSPLANTED HUMAN HEARTS FOLLOWING AUTONOMIC BLOCKADE

1. The present study was performed to test whether beat-to-beat cardio vascular control in cardiac allograft recipients resides in cholinergi c and/or adrenergic nerves that are intrinsic to the heart. 2. Heart r ate (HR) fluctuations synchronous with respiration during spontaneous, double tidal volume and metronome-synchronized breathing were quantif ied in 13 human heart transplant recipients. We also examined the effe cts of sequential cholinergic and beta-adrenoceptor (combined) autonom ic blockade on respiratory sinus arrythmia (RSA), We computed RSA ampl itude and the correlation between respiration and changes in HR (cardi opulmonary synchronization; CPS), Group means were compared using repe ated-measures analysis of variance. Transplant recipients served as th eir own controls. 3. In the basal state, moderate RSA amplitude and CP S were observed, During cholinergic and combined blockade, we observed no significant change in RSA amplitude, whereas CPS increased signifi cantly during combined blockade (P<0.05). The amplitude of RSA increas ed during respiration at double baseline tidal volume, but not at any of the other breathing manoeuvres (P<0.01). In contrast, CPS increased significantly during both patterned breathing manoeuvres, No signific ant correlation was seen between mean right atrial pressure and RSA am plitude, In 23% of subjects with low CPS, HR oscillated with arterial pressure. These oscillations were independent of respiration. During a ll three patterns of respiration, a significant inverse correlation wa s observed between CPS and pulse pressure (r = -0.53 to -0.73). Thus, as the amplitude of pulse pressure increased, respiration accounted fo r a smaller percentage of HR variation. 4. In conclusion, RSA persists and the magnitude of CPS increases following combined autonomic block ade, These studies suggest that while RSA after cardiac transplantatio n is not cholinergically or adrenergically mediated, it may be related to mechanical stretch of the sinus node caused by changes in intratho racic pressure and perfusion pressure.