Influence of central venous pressure change on plasma vasopressin in humans

1986 ◽  
Vol 61 (4) ◽  
pp. 1352-1357 ◽  
Author(s):  
P. Norsk ◽  
F. Bonde-Petersen ◽  
J. Warberg
Keyword(s):  
Central Venous Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Osmolality ◽  
Hemoglobin Concentration ◽  
Positive Pressure ◽  
Fluid Restriction ◽  
Lower Body ◽  
Central Venous ◽  
The Subject

After overnight food and fluid restriction, nine healthy males were examined before, during, and after lower body positive pressure (LBPP) of 11 +/- 1 mmHg (mean +/- SE) for 30 min and before, during, and after graded lower body negative pressure (LBNP) of -10 +/- 1, -20 +/- 2, and -30 +/- 2 mmHg for 20 min each. LBPP and LBNP were performed with the subject in the supine position in a plastic box encasing the subject from the xiphoid process and down, thus including the splanchnic area. Central venous pressure (CVP) during supine rest was 7.5 +/- 0.5 mmHg, increasing to 13.4 +/- 0.8 mmHg (P less than 0.001) during LBPP and decreasing significantly at each step of LBNP to 2.0 +/- 0.5 mmHg (P less than 0.001) at 15 min of -30 +/- 2 mmHg LBNP. Plasma arginine vasopressin (AVP) did not change significantly in face of this large variation in CVP of 11.4 mmHg. Mean arterial pressure increased significantly during LBPP from 100 +/- 2 to 117 +/- 3 Torr (P less than 0.001) and only at one point during LBNP of -30 +/- 2 mmHg from 102 +/- 1 to 115 +/- 5 mmHg (P less than 0.05). Heart rate did not change during LBPP but increased slightly from 51 +/- 3 to 55 +/- 3 beats/min (P less than 0.05) only at 7 min of LBNP of -30 +/- 2 mmHg. Plasma osmolality, sodium, and potassium did not change during the experiment. Hemoglobin concentration increased during LBPP and LBNP, whereas hematocrit only increased during LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Reflex-Mediated Reduction in Human Cerebral Blood Volume

2005 ◽  
Vol 25 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Timothy D Wilson ◽  
J Kevin Shoemaker ◽  
R Kozak ◽  
T-Y Lee ◽  
Adrian W Gelb
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Lower Body Negative Pressure ◽  
Mean Transit Time ◽  
Venous Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Lower Body ◽  
Central Venous

Adrenergic nerves innervate the human cerebrovasculature, yet the functional role of neurogenic influences on cerebral hemodynamics remains speculative. In the current study, regional cerebrovascular responses to sympathoexcitatory reflexes were evaluated. In eight volunteers, contrast-enhanced computed tomography was performed at baseline, –40 mmHg lower body negative pressure (LBNP), and a cold pressor test (CPT). Cerebral blood volume (CBV), mean transit time (MTT), and cerebral blood flow (CBF) were evaluated in cortical gray matter (GM), white matter (WM), and basal ganglia/thalamus (BGT) regions. Lower body negative pressure resulted in tachycardia and decreased central venous pressure while mean arterial pressure was maintained. Cold pressor test resulted in increased mean arterial pressure concomitant with tachycardia but no change in central venous pressure. Neither reflex altered end-tidal carbon dioxide. Cerebral blood volume was reduced in GM during both LBNP and CPT ( P<0.05) but was unchanged in WM and BGT. Mean transit time was reduced in WM and GM during CPT ( P<0.05). Cerebral blood flow was only modestly affected with either reflex ( P<0.07). The combined reductions in GM CBV (˜ –25%) and MTT, both with and without any change in central venous pressure, with small CBF changes (˜ –11%), suggest that active venoconstriction contributed to the volume changes. These data demonstrate that CBV is reduced during engagement of sympathoexcitatory reflexes and that these cerebrovascular changes are heterogeneously distributed.

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Reductions in central venous pressure by lower body negative pressure or blood loss elicit similar hemodynamic responses

2014 ◽  
Vol 117 (2) ◽  
pp. 131-141 ◽  
Author(s):  
Blair D. Johnson ◽  
Noud van Helmond ◽  
Timothy B. Curry ◽  
Camille M. van Buskirk ◽  
Victor A. Convertino ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Loss ◽  
Central Venous Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Stimulus Response ◽  
Response Slope

The purpose of this study was to compare hemodynamic and blood analyte responses to reduced central venous pressure (CVP) and pulse pressure (PP) elicited during graded lower body negative pressure (LBNP) to those observed during graded blood loss (BL) in conscious humans. We hypothesized that the stimulus-response relationships of CVP and PP to hemodynamic responses during LBNP would mimic those observed during BL. We assessed CVP, PP, heart rate, mean arterial pressure (MAP), and other hemodynamic markers in 12 men during LBNP and BL. Blood samples were obtained for analysis of catecholamines, hematocrit, hemoglobin, arginine vasopressin, and blood gases. LBNP consisted of 5-min stages at 0, 15, 30, and 45 mmHg of suction. BL consisted of 5 min at baseline and following three stages of 333 ml of hemorrhage (1,000 ml total). Individual r2 values and linear regression slopes were calculated to determine whether the stimulus (CVP and PP)-hemodynamic response trajectories were similar between protocols. The CVP-MAP trajectory was the only CVP-response slope that was statistically different during LBNP compared with BL (0.93 ± 0.27 vs. 0.13 ± 0.26; P = 0.037). The PP-heart rate trajectory was the only PP-response slope that was statistically different during LBNP compared with BL (−1.85 ± 0.45 vs. −0.46 ± 0.27; P = 0.024). Norepinephrine, hematocrit, and hemoglobin were all lower at termination in the BL protocol compared with LBNP ( P < 0.05). Consistent with our hypothesis, LBNP mimics the hemodynamic stimulus-response trajectories observed during BL across a significant range of CVP in humans.

Effect of central venous pressure on arterial baroreflex control of heart rate

1979 ◽  
Vol 236 (1) ◽  
pp. H42-H47 ◽  
Author(s):  
A. Takeshita ◽  
A. L. Mark ◽  
D. L. Eckberg ◽  
F. M. Abboud
Keyword(s):  
Central Venous Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Sinus Node ◽  
Venous Pressure ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Central Venous ◽  
Baroreceptor Stimulation ◽  
Arterial Baroreceptor

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.

Carotid baroreflex responsiveness to lower body positive pressure-induced increases in central venous pressure

1993 ◽  
Vol 265 (3) ◽  
pp. H918-H922 ◽  
Author(s):  
X. Shi ◽  
J. T. Potts ◽  
B. H. Foresman ◽  
P. B. Raven
Keyword(s):  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Baroreflex Control ◽  
Lower Body Positive Pressure ◽  
Carotid Baroreflex ◽  
Body Positive ◽  
Neck Pressure

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.

Hemodynamic responses to graded lower body positive pressure

1993 ◽  
Vol 265 (1) ◽  
pp. H69-H73 ◽  
Author(s):  
X. Shi ◽  
C. G. Crandall ◽  
P. B. Raven
Keyword(s):  
Forearm Blood Flow ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Intramuscular Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Pressure Sensitive ◽  
Body Positive ◽  
Forearm Vascular Resistance

Fourteen healthy young men were exposed to progressive increases in lower body positive pressure (LBPP) from 0 to 40 Torr in the supine position. Central venous pressure (CVP) increased 1.09 mmHg (P < 0.05) at 5 Torr LBPP. Between 20 and 40 Torr LBPP CVP increased 0.85 mmHg, resulting in a total increase of 2.06 mmHg (P < 0.05). During 0–20 Torr LBPP mean arterial pressure (MAP) increased from 86 to 89 mmHg with a slope of 0.15 mmHg/Torr LBPP. Stroke volume and cardiac output were significantly increased at 20 Torr LBPP. Beyond 20 Torr LBPP, MAP increased to 95 mmHg at 40 Torr (P < 0.05) with a slope of 0.32 mmHg/Torr LBPP. Forearm blood flow increased above rest at 40 Torr LBPP (P< 0.05). However, neither peripheral nor forearm vascular resistance decreased significantly from rest. Despite the significant increases in MAP, heart rate was unchanged above 20 Torr LBPP. These data suggest that LBPP produces increases in CVP at 0–20 Torr by translocation of blood volume from the legs to the thorax. At LBPP > 20 Torr, further increases in CVP and MAP were produced by other mechanisms possibly related to an activation of intramuscular pressure-sensitive receptors.

Increase in vagal activity during hypotensive lower-body negative pressure in humans

1988 ◽  
Vol 255 (1) ◽  
pp. R149-R156 ◽  
Author(s):  
K. Sander-Jensen ◽  
J. Mehlsen ◽  
C. Stadeager ◽  
N. J. Christensen ◽  
J. Fahrenkrug ◽  
...  
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Initial Increase ◽  
Vagal Activity ◽  
Lower Body ◽  
Central Venous ◽  
Subsequent Decrease ◽  
Before And After

Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)

ANP-mediated volume depletion attenuates renal responses in humans

1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Urine Volume ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Central Venous

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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