Krediet, C. T. Paul

On a beat‐by‐beat basis, withdrawal of baroreflex inhibition results in a burst of (muscle) sympathetic nerve activity (MSNA) as well as a decrease in the cardiac interval due to vagal withdrawal. The aim of this study was to quantify the cardiac and vascular components of the hemodynamic response following individual bursts of MSNA. We measured MSNA (peroneal microneurography), arterial pressure (AP, directly) and cardiac output (CO, acetylene uptake) in 11 healthy supine subjects. Beat‐by‐beat CO was also derived by arterial pulse wave analysis (Modelflow) and calibrated to the measured CO. Total peripheral resistance (TPR) was calculated as meanAP/CO. For each subject, the mean change in diastolic AP, inter‐beat interval (IBI), CO and TPR were calculated for each of 15 cardiac cycles following a burst of MSNA. We found a transient increase in diastolic AP (1.9±.34 mmHg), CO (.097±.026 l/min) and TPR (.023±.007 mmHg/l/min) and a transient shortening of IBI (−16±4 ms). Maxima occurred 5.8, 2.7, 6.1 and 2.6 s, respectively, after the beat that triggered the burst. There was a linear relation between MSNA (burst incidence) at baseline and time to maximum AP increase (r=.75, p=.008) as well as to time to maximum TPR (r=.69, p=.01). This suggests that subjects with higher resting MSNA have delayed hemodynamic responses following individual bursts. Support: NIH NS32352, NL Heart Found. 2004/T007, Fulbright program