Atrial natriuretic factor and central venous pressure during intermittent and continuous lower-body positive pressure in healthy humans

1990 ◽  
Vol 10 (3) ◽  
pp. 245-255 ◽  
Author(s):  
N. Kellers
Keyword(s):  
Central Venous Pressure ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Healthy Humans ◽  
Natriuretic Factor ◽  
Body Positive

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)

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.

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 Lower Body Positive Pressure Application with an Antigravity Suit in Acute Carotid Occlusion

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Karine Berthet ◽  
Anne Claire Lukaszewicz ◽  
Marie-Germaine Bousser ◽  
Didier Payen
Keyword(s):  
Potential Risk ◽  
Venous Pressure ◽  
Carotid Occlusion ◽  
Positive Pressure ◽  
Lower Body ◽  
Lower Body Positive Pressure ◽  
Risk Of Bleeding ◽  
Clinical Recovery ◽  
Pressure Application ◽  
Body Positive

The challenge in acute stroke is still to reperfuse as early as possible the ischemic territory. Since fibrinolytic therapies have a limited window with potential risk of bleeding, having a nonpharmacologic mean to recruit vessels in area surrounding necrosis might be useful. We propose here to use antigravity suit inflated at “venous” pressure levels to shift blood towards thoracic and brain territories. We report two cases of spectacular clinical recovery after acute carotid occlusion.

Effect of increased intracardiac and arterial pressure on plasma vasopressin in humans

1984 ◽  
Vol 246 (5) ◽  
pp. H647-H651 ◽  
Author(s):  
S. R. Goldsmith ◽  
A. W. Cowley ◽  
G. S. Francis ◽  
J. N. Cohn
Keyword(s):  
Heart Rate ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Water Restriction ◽  
Lower Body Positive Pressure ◽  
Arterial Blood ◽  
Body Positive ◽  
Cardiopulmonary Receptors

The effects of loading cardiopulmonary and sinoaortic baroreceptors on plasma arginine vasopressin (AVP) levels were examined in 18 healthy young adults after a mild water restriction. Cardiopulmonary receptors were acutely loaded by volume expansion which increased central venous pressure (CVP) from 4.7 +/- 1.9 to 7.3 +/- 2.2 mmHg but did not change mean arterial blood pressure (MAP). Both receptor groups were acutely loaded by applications of lower body positive pressure, which induced a comparable increase in CVP and, in addition, raised MAP from 85 +/- 6.7 to 93 +/- 6.8 mmHg (P less than 0.001). There was evidence of reflex activation as forearm blood flow and heart rate increased during volume expansion while the increase in heart rate was blocked during lower body positive pressure. Neither intervention significantly altered the control AVP level of 4.6 +/- 1.4 pg/ml. An investigation of more prolonged stimulation of cardiopulmonary receptors was carried out using 1 h of head-down tilt. Again, despite increases in CVP (5.1 +/- 1.3 to 9.0 +/- 1.4 mmHg, P less than 0.005), AVP (5.7 +/- 2.4 pg/ml) did not decrease. MAP did not change during head-down tilt. There were no changes in osmolality throughout any of the studies. AVP levels in humans are therefore not responsive to moderate isosmotic loading of the cardiopulmonary and sinoaortic baroreceptors under conditions of mild water restriction.

Interaction of central venous pressure, intramuscular pressure, and carotid baroreflex function

1997 ◽  
Vol 272 (3) ◽  
pp. H1359-H1363 ◽  
Author(s):  
X. Shi ◽  
B. H. Foresman ◽  
P. B. Raven
Keyword(s):  
Central Venous Pressure ◽  
Venous Pressure ◽  
Chamber Pressure ◽  
Positive Pressure ◽  
Intramuscular Pressure ◽  
Central Venous ◽  
Total Blood ◽  
Lower Body Positive Pressure ◽  
Carotid Baroreflex ◽  
Maximal Gain

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.

scholarly journals Effect of Uphill Running on VO2, Heart Rate and Lactate Accumulation on Lower Body Positive Pressure Treadmills

Sports ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 51
Author(s):  
Daniel Fleckenstein ◽  
Olaf Ueberschär ◽  
Jan C. Wüstenfeld ◽  
Peter Rüdrich ◽  
Bernd Wolfarth
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Body Weight Support ◽  
Positive Pressure ◽  
Lower Body ◽  
Lactate Accumulation ◽  
Biomechanical Stress ◽  
Lower Body Positive Pressure ◽  
Weight Support ◽  
Body Positive

Lower body positive pressure treadmills (LBPPTs) as a strategy to reduce musculoskeletal load are becoming more common as part of sports conditioning, although the requisite physiological parameters are unclear. To elucidate their role, ten well-trained runners (30.2 ± 3.4 years; VO2max: 60.3 ± 4.2 mL kg−1 min−1) ran at 70% of their individual velocity at VO2max (vVO2max) on a LBPPT at 80% body weight support (80% BWSet) and 90% body weight support (90% BWSet), at 0%, 2% and 7% incline. Oxygen consumption (VO2), heart rate (HR) and blood lactate accumulation (LA) were monitored. It was found that an increase in incline led to increased VO2 values of 6.8 ± 0.8 mL kg−1 min−1 (0% vs. 7%, p < 0.001) and 5.4 ± 0.8 mL kg−1 min−1 (2% vs. 7%, p < 0.001). Between 80% BWSet and 90% BWSet, there were VO2 differences of 3.3 ± 0.2 mL kg−1 min−1 (p < 0.001). HR increased with incline by 12 ± 2 bpm (0% vs. 7%, p < 0.05) and 10 ± 2 bpm (2% vs. 7%, p < 0.05). From 80% BWSet to 90% BWSet, HR increases of 6 ± 1 bpm (p < 0.001) were observed. Additionally, LA values showed differences of 0.10 ± 0.02 mmol l−1 between 80% BWSet and 90% BWSet. Those results suggest that on a LBPPT, a 2% incline (at 70% vVO2max) is not yet sufficient to produce significant physiological changes in VO2, HR and LA—as opposed to running on conventional treadmills, where significant changes are measured. However, a 7% incline increases VO2 and HR significantly. Bringing together physiological and biomechanical factors from previous studies into this practical context, it appears that a 7% incline (at 80% BWSet) may be used to keep VO2 and HR load unchanged as compared to unsupported running, while biomechanical stress is substantially reduced.

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