scholarly journals Transient effects of carotid baroreflex stimulation via the neck chamber device on central venous pressure

Author(s):  
Fosca Quarti‐Trevano ◽  
Gino Seravalle ◽  
Domenico Spaziani ◽  
Jennifer Vanoli ◽  
Giuseppe Mancia ◽  
...  
1989 ◽  
Vol 257 (5) ◽  
pp. H1389-H1395 ◽  
Author(s):  
J. A. Pawelczyk ◽  
P. B. Raven

To test the hypothesis that unloading cardiopulmonary receptors improves human carotid baroreceptor responsiveness we measured heart rate (HR) and mean radial artery blood pressure (BP) responses elicited by trains of neck pressure and neck suction from +40 to -65 Torr during graded lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 Torr in eight healthy men. Gain of the carotid baroreflexes was determined from logistic modeling of the HR [expressed as R-R interval (RRI)] and BP responses to neck pressure and neck suction. Central venous pressure (CVP) decreased progressively from control values of 6.2 +/- 0.6 (SE) Torr to -0.8 +/- 0.1 Torr at -50 Torr LBNP (P less than 0.001). HR changed little from control values of 62.7 +/- 2.1 beat/min to 65.9 +/- 2.8 beat/min at -15 Torr (P = NS), but increased significantly to 80.6 +/- 2.6 beats/min at -50 Torr (P less than 0.001). Maximum gain of the HR and BP stimulus-response curves was linearly and inversely related to decreases in CVP and could be described by the relationships Max RRI gain = -0.694 (CVP) + 11.6 [r2 = 0.94, standard error of estimate (SEE) = 0.45, P less than 0.001] and Max BP gain = -0.0292 (CVP) + 0.391 (r2 = 0.81, SEE = 0.038, P less than 0.001). We suggest that reductions in central venous pressure and/or central blood volume augment both HR and BP carotid baroreflex responses in man by reducing an inhibitory influence from cardiopulmonary receptors.


1993 ◽  
Vol 265 (3) ◽  
pp. H918-H922 ◽  
Author(s):  
X. Shi ◽  
J. T. Potts ◽  
B. H. Foresman ◽  
P. B. Raven

Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.


1997 ◽  
Vol 272 (3) ◽  
pp. H1359-H1363 ◽  
Author(s):  
X. Shi ◽  
B. H. Foresman ◽  
P. B. Raven

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 (Gmax) 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. Gmax 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 Gmax of the carotid baroreflex of HR and MAP was significantly decreased during LBPP by -0.145 +/- 0.039 beats x min(-1) x mmHg(-1) (38%) and -0.071 +/- 0.013 mmHg/mmHg (25%), respectively; however, VE-I did not affect Gmax. During VE-II, CVP was significantly greater than that elicited by LBPP, and the Gmax 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.


2006 ◽  
Vol 0 (0) ◽  
Author(s):  
Aline S. C. Belela ◽  
Mavilde L. G. Pedreira ◽  
Maria Angélica S. Peterlini ◽  
Denise M. Kusahara ◽  
Werther B. Carvalho ◽  
...  

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