INTERACTION OF CENTRAL VENOUS-PRESSURE, INTRAMUSCULAR PRESSURE, AND CAROTID BAROREFLEX FUNCTION

Seven healthy volunteer men participated in an experiment involving lo wer body positive pressure (LBPP) of 30 Torr and acute volume expansio ns of 5-6% (VE-I) and 9-10% (VE-II) of their total blood volume (TBV) to differentiate the effect of increased intramuscular pressure and ce ntral venous pressure (CVP) on the maximal gain (G(max)) of the caroti d baroreflex. During each experimental condition, the heart rate (HR), mean arterial pressure (MAP; intraradial artery or Finapres), and CVP (at the 3rd-4th intercostal space) were monitored continuously. G(max ) was derived from the logistic modeling of the HR and MAP responses t o ramped changes in carotid sinus transmural pressure using a protocol of pulsatile changes in neck chamber pressure from +40 to -65 Torr. T he increase in CVP during +3O-Torr LBPP was 1.5 mmHg (P < 0.05) and wa s similar to that observed during VE-I (1.7 mmHg, P > 0.05). The G(max ) of the carotid baroreflex of HR and MAP was significantly decreased during LBPP by -0.145 +/- 0.039 beats . min(-1). mmHg(-1) (38%) and -0 .071 +/- 0.013 mmHg/mmHg (25%), respectively; however, VE-I did not af fect G(max). During VE-II, CVP was significantly greater than that eli cited by LBPP, and the G(max) of the carotid baroreflex of the HR and MAP responses was significantly reduced. We conclude that carotid baro reflex responsiveness was selectively inhibited by increasing intramus cular pressure, possibly resulting in an activation of the intramuscul ar mechanoreceptors during LBPP. Furthermore, it would appear that the inhibition of the carotid baroreflex, via cardiopulmonary barorecepto r loading (increased CVP), occurred when a threshold pressure (CVP) wa s achieved.