TY - JOUR
T1 - Interaction of central venous pressure, intramuscular pressure, and carotid baroreflex function
AU - Shi, Xiangrong
AU - Foresman, Brian H.
AU - Raven, Peter B.
PY - 1997/3
Y1 - 1997/3
N2 - Seven healthy volunteer men participated in an experiment involving lower body positive pressure (LBPP) of 30 Torr and acute volume expansions 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 central venous pressure (CVP) on the maximal gain (G(max)) of the carotid 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 to ramped changes in carotid sinus transmural pressure using a protocol of pulsatile changes in neck chamber pressure from +40 to -65 Torr. The increase in CVP during +30-Torr LBPP was 1.5 mmHg (P < 0.05) and was 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 affect G(max). During VE-II, CVP was significantly greater than that elicited by LBPP, and the G(max) of the carotid baroreflex of the HR and MAP responses was significantly reduced. We conclude that carotid baroreflex responsiveness was selectively inhibited by increasing intramuscular pressure, possibly resulting in an activation of the intramuscular mechanoreceptors during LBPP. Furthermore, it would appear that the inhibition of the carotid baroreflex, via cardiopulmonary baroreceptor loading (increased CVP), occurred when a threshold pressure (CVP) was achieved.
AB - Seven healthy volunteer men participated in an experiment involving lower body positive pressure (LBPP) of 30 Torr and acute volume expansions 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 central venous pressure (CVP) on the maximal gain (G(max)) of the carotid 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 to ramped changes in carotid sinus transmural pressure using a protocol of pulsatile changes in neck chamber pressure from +40 to -65 Torr. The increase in CVP during +30-Torr LBPP was 1.5 mmHg (P < 0.05) and was 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 affect G(max). During VE-II, CVP was significantly greater than that elicited by LBPP, and the G(max) of the carotid baroreflex of the HR and MAP responses was significantly reduced. We conclude that carotid baroreflex responsiveness was selectively inhibited by increasing intramuscular pressure, possibly resulting in an activation of the intramuscular mechanoreceptors during LBPP. Furthermore, it would appear that the inhibition of the carotid baroreflex, via cardiopulmonary baroreceptor loading (increased CVP), occurred when a threshold pressure (CVP) was achieved.
KW - blood volume
KW - gain
KW - lower body positive pressure
KW - mechanoreceptor
UR - http://www.scopus.com/inward/record.url?scp=33751279423&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.1997.272.3.h1359
DO - 10.1152/ajpheart.1997.272.3.h1359
M3 - Article
C2 - 9087612
AN - SCOPUS:33751279423
SN - 0363-6135
VL - 272
SP - H1359-H1363
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 3 41-3
ER -