Influence of central venous pressure change on plasma vasopressin in humans

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)     

Human cardiovascular reactions to simulated hypovolaemia, modified by the opiate antagonist naloxone

Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg.kg-1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP = 40 mm Hg increased from 60.0 +/- 4.8 mm Hg to 64.8 +/- 4.1 mm Hg (N = 4, p less than 0.02) and LVETI at LBNP = 20 mm Hg increased from 384.4 +/- 5.2 ms to 396.8 +/- 6.2 ms (N = 6, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of lymphatic outflow pressure on lymphatic albumin transport in humans.

The effects of posture on the lymphatic outflow pressure and lymphatic return of albumin were examined in 10 volunteers. Lymph flow was stimulated with a bolus infusion of isotonic saline (0.9%, 12.6 ml/kg body wt) under four separate conditions: upright rest (Up), upright rest with lower body positive pressure (LBPP), supine rest (Sup), and supine rest with lower body negative pressure (LBNP). The increase in plasma albumin content (Delta Alb) during the 2 h after bolus saline infusion was greater in Up than in LBPP: 82.9 +/- 18.5 vs. -28.4 mg/kg body wt. Delta Alb was greater in LBNP than in Sup: 92.6 vs. -22.5 +/- 18.9 mg/kg body wt (P < 0.05). The greater Delta Alb in Up and Sup with LBNP were associated with a lower estimated lymphatic outflow pressure on the basis of the difference in central venous pressure (Delta CVP). During LBPP, CVP was increased compared with Up: 3.8 +/- 1.4 vs. -1.2 +/- 1.2 mmHg. During LBNP, CVP was reduced compared with Sup: -3.0 +/- 2.2 vs. 1.7 +/- 1.0 mmHg. The translocation of protein into the vascular space after bolus saline infusion reflects lymph return of protein and is higher in Up than in Sup. Modulation of CVP with LBPP or LBNP in Up and Sup, respectively, reversed the impact of posture on lymphatic outflow pressure. Thus posture-dependent changes in lymphatic protein transport are modulated by changes in CVP through its mechanical impact on lymphatic outflow pressure.     

Hyperhydration with glycerol solutions

Glycerol was tested as an agent to promote hyperhydration of male and female subjects. Series I experiments involved ingesting 0.5, 1.0, or 1.5 g glycerol/kg body wt and within 40 min drinking 0.1% NaCl, 21.4 ml/kg. In series II, 1.0 g glycerol/kg body wt was ingested at time 0, and 25.7 ml/kg of 0.1% NaCl was ingested over a 3.5-h period. Experiments were of 4-h duration and included controls without glycerol as each subject served as his/her control. Blood samples were taken at 40- or 60-min intervals for hemoglobin (Hb), hematocrit (Hct), plasma osmolality, glycerol, and multiple blood chemistry analyses. Urine was collected at 60-min intervals. Glycerol ingestion increased plasma osmolality for 2 h and reduced the total 4-h urine volume. There were no significant changes in Hb or Hct as a result of the glycerol or excess fluid intake. This study demonstrates that glycerol plus excess fluid intake can produce hyperhydration for at least 4 h.     

Cardiovascular responses to apneic facial immersion during altered cardiac filling.

The hypothesis that reduced cardiac filling, as a result of lower body negative pressure (LBNP) and postexercise hypotension (PEH), would attenuate the reflex changes to heart rate (HR), skin blood flow (SkBF), and mean arterial pressure (MAP) normally induced by facial immersion was tested. The purpose of this study was to investigate the cardiovascular control mechanisms associated with apneic facial immersion during different cardiovascular challenges. Six subjects randomly performed 30-s apneic facial immersions in 6.0 +/- 1.2 degrees C water under the following conditions: 1) -20 mmHg LBNP, 2) +40 mmHg lower body positive pressure (LBPP), 3) during a period of PEH, and 4) normal resting (control). Measurements included SkBF at one acral (distal phalanx of the thumb) and one nonacral region of skin (ventral forearm), HR, and MAP. Facial immersion reduced HR and SkBF at both sites and increased MAP under all conditions (P < 0.05). Reduced cardiac filling during LBNP and PEH significantly attenuated the absolute HR nadir observed during the control immersion (P < 0.05). The LBPP condition did not result in a lower HR nadir than control but did result in a nadir significantly lower than that of the LBNP and PEH conditions (P < 0.05). No differences were observed in either SkBF or MAP between conditions; however, the magnitude of SkBF reduction was greater at the acral site than at the nonacral site for all conditions (P < 0.05). These results suggest that the cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised.     

Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humans

Orthostatic tolerance is reduced in the heat-stressed human. This study tested the following hypotheses: 1) whole body heat stress reduces cerebral blood velocity (CBV) and increases cerebral vascular resistance (CVR); and 2) reductions in CBV and increases in CVR in response to an orthostatic challenge will be greater while subjects are heat stressed. Fifteen subjects were instrumented for measurements of CBV (transcranial ultrasonography), mean arterial blood pressure (MAP), heart rate, and internal temperature. Whole body heating increased both internal temperature (36.4+/-0.1 to 37.3+/-0.1 degrees C) and heart rate (59+/-3 to 90+/-3 beats/min); P<0.001. Whole body heating also reduced CBV (62+/-3 to 53+/-2 cm/s) primarily via an elevation in CVR (1.35+/-0.06 to 1.63+/-0.07 mmHg.cm-1.s; P<0.001. A subset of subjects (n=8) were exposed to lower-body negative pressure (LBNP 10, 20, 30, 40 mmHg) in both normothermic and heat-stressed conditions. During normothermia, LBNP of 30 mmHg (highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBV, CVR, or MAP. During whole body heating, this LBNP decreased MAP (81+/-2 to 75+/-3 mmHg), decreased CBV (50+/-4 to 39+/-1 cm/s), and increased CVR (1.67+/-0.17 to 1.92+/-0.12 mmHg.cm-1.s); P<0.05. These data indicate that heat stress decreases CBV, and the reduction in CBV for a given orthostatic challenge is greater during heat stress. These outcomes reduce the reserve to buffer further decreases in cerebral perfusion before presyncope. Increases in CVR during whole body heating, coupled with even greater increases in CVR during orthostasis and heat stress, likely contribute to orthostatic intolerance.     

'Neutral point titration': cardiovascular regulation during combined (LBNP/HDT vs. LBPP/HUT) stimulation

This study was undertaken to identify combinations ('neutral points', NP) of orthostatic (tilt: head-down = HDT, head-up = HUT) and pseudo-orthostatic (lower body pressure: positive = LBPP, negative = LBNP) stimuli able to compensate one another in their effect on hemodynamic variables, electrical thoracic impedance (TI), hematocrit and plasma mass density (PD), and blood hormone concentrations. We asked if NP's exist for tested variables (hypothesis 1), if NP's differ with variables (hypothesis 2), and if NP's change as a function of time (hypothesis 3). For the blood volume sensitive variables (PD, plasma total protein concentration, and hematocrit) we found a NP at > or = 30 degrees HDT at LBNP-35 and -15 degrees HUT with LBPP+35. There was no clear PD / total plasma protein concentration effect with various degrees of LBNP-15 / HDT. NP's could be derived for some hemodynamic variables: With LBNP-35, a NP for heart rate was derived at -25 degrees HDT and for MAP at -30 degrees HDT. Heart rate intersected at > or = 30 degrees HDT with LBNP-15 (extrapolated), stroke volume index (SVI) at -20 degrees HDT. With LBPP+35, SVI had its NP at 11 degrees HUT. The hormonal responses displayed a pattern where plasma renin activity (PRA) NP's were logically scattered with LBNP intensity, whereas aldosterone displayed similar NP's with both LBNP intensities.     

Effect of lower-body positive pressure on postural fluid shifts in men

To quantify the effect of 60 mm Hg lower-body positive pressure (LBPP) on orthostatic blood-volume shifts, the mass densities (+/- 0.1 g.1-1) of antecubital venous blood and plasma were measured in five men (27-42 years) during combined tilt table/antigravity suit inflation and deflation experiments. The densities of erythrocytes, whole-body blood, and of the shifted fluid were computed and the magnitude of fluid and protein shifts were calculated during head-up tilt (60 degrees) with and without application of LBPP. During 30-min head-up tilt with LBPP, blood density (BD) and plasma density (PD) increased by 1.6 +/- 0.3 g.1-1, and by 0.8 +/- 0.2 g.1-1 (+/- SD) (N = 9), respectively. In the subsequent period of tilt without LBPP, BD and PD increased further to + 3.6 +/- 0.9 g.1-1, and to + 2.0 +/- 0.7 g.1-1 (N = 7), compared to supine control. The density increases in both periods were significant (p less than 0.05). Erythrocyte density remained unaltered with changes in body position and pressure suit inflation/deflation. Calculated shifted-fluid densities (FD) during tilt with LBPP (1006.0 +/- 1.1 g.1-1, N = 9), and for subsequent tilt after deflation (1002.8 +/- 4.1 g.1-1, N = 7) were different from each other (p less than 0.03). The plasma volume decreased by 6.0 +/- 1.2% in the tilt-LBPP period, and by an additional 6.4 +/- 2.7% of the supine control level in the subsequent postdeflation tilt period. The corresponding blood volume changes were 3.7 +/- 0.7% (p less than 0.01), and 3.5 +/- 2.1% (p less than 0.05), respectively. Thus, about half of the postural hemo-concentration occurring during passive head-up tilt was prevented by application of 60 mm Hg LBPP.     

Ambulation in simulated fractional gravity using lower body positive pressure: cardiovascular safety and gait analyses.

The purpose of this study is to assess cardiovascular responses to lower body positive pressure (LBPP) and to examine the effects of LBPP unloading on gait mechanics during treadmill ambulation. We hypothesized that LBPP allows comfortable unloading of the body with minimal impact on the cardiovascular system and gait parameters. Fifteen healthy male and female subjects (22-55 yr) volunteered for the study. Nine underwent noninvasive cardiovascular studies while standing and ambulating upright in LBPP, and six completed a gait analysis protocol. During stance, heart rate decreased significantly from 83 +/- 3 beats/min in ambient pressure to 73 +/- 3 beats/min at 50 mmHg LBPP (P < 0.05). During ambulation in LBPP at 3 mph (1.34 m/s), heart rate decreased significantly from 99 +/- 4 beats/min in ambient pressure to 84 +/- 2 beats/min at 50 mmHg LBPP (P < 0.009). Blood pressure, brain oxygenation, blood flow velocity through the middle cerebral artery, and head skin microvascular blood flow did not change significantly with LBPP. As allowed by LBPP, ambulating at 60 and 20% body weight decreased ground reaction force (P < 0.05), whereas knee and ankle sagittal ranges of motion remained unaffected. In conclusion, ambulating in LBPP has no adverse impact on the systemic and head cardiovascular parameters while producing significant unweighting and minimal alterations in gait kinematics. Therefore, ambulating within LBPP is potentially a new and safe rehabilitation tool for patients to reduce loads on lower body musculoskeletal structures while preserving gait mechanics.     

The cardiovascular response to lower body negative pressure in humans depends on seal location

We tested whether seal location at iliac crest (IC) or upper abdomen (UA), before and during lower body negative pressure (LBNP), would affect thoracic electrical impedance, hepatic blood flow, and central cardiovascular responses to LBNP. After 30 min of supine rest, LBNP at -40 mm Hg was applied for 15 min, either at IC or UA, in 14 healthy males. Plasma density and indocyanine green concentrations assessed plasma volume changes and hepatic perfusion. With both sealing types, LBNP-induced effects remained unchanged for mean arterial pressure (-3.0+/-1.1 mm Hg), cardiac output (-1.0 l min(-1)), and plasma volume (-11 %). Heart rate was greater during UA (80.6+/-3.3 bpm) than IC (76.0+/-2.5 bpm) (p<0.01) and thoracic impedance increased more using UA (3.2+/-0.2 Omega) than IC (1.8+/-0.2 Omega) (p<0.0001). Furthermore, during supine rest, UA was accompanied by lower thoracic impedance (26.9+/-1.1 vs 29.0+/-0.8 Omega, p<0.001) and hepatic perfusion (1.6 vs 1.8 l.min(-1), p<0.05) compared to IC. The data suggest that the reduction in central blood volume in response to LBNP depends on location of the applied seal. The sealing in itself altered blood volume distribution and hepatic perfusion in supine resting humans. Finally, application of LBNP with the seal at the upper abdomen induced a markedly larger reduction in central blood volume and greater increases in heart rate than when the seal was located at the iliac crest.     

Zinc: an inhibitor of prolactin (PRL) secretion in humans

The response of plasma prolactin (PRL) to oral administration of increasing doses of zinc (25.0, 37.5 and 50.0 mg) was studied in 17 normal adult men and women. Blood samples were collected at 10 and 30-min intervals over a period of 120 min after two basal times (-30 and 0 min). PRL concentrations significantly fell below basal levels in all subjects in response to the increase in plasma zinc levels, as compared to the controls. These results suggest that acute hyperzincemia can inhibit basal PRL secretion in normal individuals.     

Compensatory reactions during lower body negative pressure (LBNP) exposure, head-up tilt (HUT) and +Gz tolerance

The effects of lower body negative pressure (LBNP) on acceleration tolerance and head-up tilt were investigated. Healthy male subjects underwent LBNP protocols of various pressures and acceleration tolerance tests; some subjects additionally underwent head-up tilt tests. All subjects were measured for hemodynamic changes and plasma hormonal level changes. The results of these studies showed acceleration tolerance to depend on plasma renin activity, left ventricular ejection time, cardiac output, preejection period, plasma aldosterone levels, and heart rate. The significance of this result is discussed.     

Hyperthermia modifies muscle metaboreceptor and baroreceptor modulation of heat loss in humans

The relative influence of muscle metabo- and baroreflex activity on heat loss responses during post-isometric handgrip (IHG) exercise ischemia remains unknown, particularly under heat stress. Therefore, we examined the separate and integrated influences of metabo- and baroreceptor-mediated reflex activity on sweat rate and cutaneous vascular conductance (CVC) under increasing levels of hyperthermia. Twelve men performed 1 min of IHG exercise at 60% of maximal voluntary contraction followed by 2 min of ischemia with simultaneous application of lower body positive pressure (LBPP, +40 mmHg), lower body negative pressure (LBNP, -20 mmHg), or no pressure (control) under no heat stress. On separate days, trials were repeated under heat stress conditions of 0.6°C (moderate heat stress) and 1.4°C (high heat stress) increase in esophageal temperature. For all conditions, mean arterial pressure was greater with LBPP and lower with LBNP than control during ischemia (all P ≤ 0.05). No differences in sweat rate were observed between pressure conditions, regardless of the level of hyperthermia (P > 0.05). Under moderate heat stress, no differences in CVC were observed between pressure conditions. However, under high heat stress, LBNP significantly reduced CVC by 21 ± 4% (P ≤ 0.05) and LBPP significantly elevated CVC by 14 ± 5% (P ≤ 0.05) relative to control. These results show that sweating during post-IHG exercise ischemia is activated by metaboreflex stimulation, and not by baroreflexes. In contrast, our results suggest that baroreflexes can influence the metaboreflex modulation of CVC, but only at greater levels of hyperthermia.     

Sustained increases in sympathetic outflow during prolonged lower body negative pressure in humans

The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of daily hyperhydration on fluid-electrolyte changes in endurance-trained volunteers during prolonged restriction of muscular activity

The aim of this investigation was to evaluate the effect of a daily intake of fluid and salt supplementation on fluid and electrolyte losses in endurance-trained volunteers during prolonged restriction of muscular activity (hypokinesia). The studies were performed on 30 long-distance runners aged 23–26 who had a peak oxygen uptake of 65.5 mL/kg/min and had taken 13.8 km/d on average prior to their participation in the study. The volunteers were divided into three groups: The volunteers in the first group were placed under normal ambulatory conditions (control subjects), the second group of volunteers subjected to hypokinesia alone (hypokinetic subjects), and the third group of volunteers was submitted to HK and consumed daily 0.1 g sodium chloride (NaCl)/kg body wt and 26 mL water/kg body wt (hyperhydrated subjects). The second and third group of volunteers were kept under an average of 2.7 km/d for 364 d. During the pre-experimental period of 60 d and during the experimental period of 364 d sodium, potassium, calcium, and magnesium in urine and plasma were determined. Blood was also assayed for osmolality, hemoglobin, hematocrit, plasma volume, plasma renin activity and plasma aldosterone. Mean arterial blood pressure was also determined. In the hyperhydrated volunteers plasma volume and arterial blood pressure increased, whereas plasma osmolality, plasma renin activity, plasma aldosterone, hematocrit, hemoglobin concentration, and urinary excretion and concentrations of electrolytes in plasma decreased. In the hypokinetic volunteers, plasma volume and arterial blood pressure decreased significantly, whereas hematocrit values, hemoglobin concenfration, plasma osmolality, plasma renin activity, plasma aldosterone, and electrolytes in urine and plasma increased significantly during the experimental period. It was concluded that chronic hyperhydration may be used in minimizing fluid and electrolyte losses in endurance-trained volunteers during prolonged restriction of muscular activity.     

Hemodynamic and neuroendocrine predictors of lower body negative pressure (LBNP) intolerance in healthy young men.

Exposure to LBNP results in body fluid shift to lower extremities similarly as under influence of orthostatic stress. In susceptible persons it leads to syncope. For better understanding why certain individuals are more susceptible to orthostatic challenges it seemed necessary to collect more data on hemodynamic and neuroendocrine adjustments occurring before onset of presyncopal symptoms Accordingly, in this study heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (CO), hematocrit, plasma catecholamines, adrenomedullin, ACTH and plasma renin activity (PRA) were measured in 24 healthy men during graded LBNP (-15, -30 and -50 mmHg). Thirteen subjects completed the test (HT group) whereas 11 had presyncope signs or symptoms at -30 mmHg or at the beginning of -50 mmHg (LT group). Comparison of these groups showed that LT subjects had lower baseline total peripheral resistance and higher plasma adrenomedullin. During LBNP plasma catecholamine and PRA increases were even greater in LT than in HT group while plasma adrenomedullin elevations were similar in both groups. Plasma ACTH increased only in LT group following presyncope symptoms. Low tolerant group showed more rapid decline of SV and CO than HT subjects from the beginning of LBNP. It is suggested that measurements of SV at the level of LBNP which did not evoke any adverse symptoms may be of predictive value for lower orthostatic tolerance.     

Metabolic, body temperature and hormonal responses to repeated periods of prolonged cycle-ergometer exercise in men.

This study was designed to find out whether rest intervals and prevention of dehydration during prolonged exercise inhibit a drift in metabolic rate, body temperature and hormonal response typically occurring during continuous work. For this purpose in ten healthy men the heart rate (fc), rectal temperature (Tre), oxygen uptake (VO2), as well as blood metabolite and some hormone concentrations were measured during 2-h exercise at approximately 50% maximal oxygen uptake split into four equal parts by 30-min rest intervals during which body water losses were replaced. During each 30-min exercise period there was a rapid change in Tre and fc superimposed on which, these values increased progressively in consecutive exercise periods (slow drift). The VO2 showed similar changes but there were no significant differences in the respiratory exchange ratio, pulmonary ventilation, mechanical efficiency and plasma osmolality between successive periods of exercise. Blood glucose, insulin and C-peptide concentrations decreased in consecutive exercise periods, whereas plasma free fatty acid, glycerol, catecholamine, growth hormone and glucagon concentrations increased. Blood lactate concentrations did not show any regular drift and the plasma cortisol concentration decreased during the first two exercise periods and then increased. In conclusion, in spite of the relatively long rest intervals between the periods of prolonged exercise and the prevention of dehydration several physiological and hormonal variables showed a distinct drift with time. It is suggested that the slow drift in metabolic rate could have been attributable in the main to the increased concentrations of heat liberating hormones.     

Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume

Upright posture and lower body negative pressure (LBNP) both induce reductions in central blood volume. However, regional circulatory responses to postural changes and LBNP may differ. Therefore, we studied regional blood flow and blood volume changes in 10 healthy subjects undergoing graded lower-body negative pressure (-10 to -50 mmHg) and 8 subjects undergoing incremental head-up tilt (HUT; 20 degrees , 40 degrees , and 70 degrees ) on separate days. We continuously measured blood pressure (BP), heart rate, and regional blood volumes and blood flows in the thoracic, splanchnic, pelvic, and leg segments by impedance plethysmography and calculated regional arterial resistances. Neither LBNP nor HUT altered systolic BP, whereas pulse pressure decreased significantly. Blood flow decreased in all segments, whereas peripheral resistances uniformly and significantly increased with both HUT and LBNP. Thoracic volume decreased while pelvic and leg volumes increased with HUT and LBNP. However, splanchnic volume changes were directionally opposite with stepwise decreases in splanchnic volume with LBNP and stepwise increases in splanchnic volume during HUT. Splanchnic emptying in LBNP models regional vascular changes during hemorrhage. Splanchnic filling may limit the ability of the splanchnic bed to respond to thoracic hypovolemia during upright posture.     

Central transmural venous pressure and plasma arginine vasopressin during negative pressure breathing in man

After overnight food and fluid restriction, 8 normal healthy males were examined in the upright sitting position before (prestudy), during and after (recovery) negative pressure breathing (NPB) with a pressure (P = difference between airway pressure and barometric pressure) of -9.6 +/- 0.5 to -10.4 +/- 0.4 mm Hg for 30 min. Plasma arginine vasopressin (pAVP) did not change significantly comparing prestudy with 10 and 30 min of NPB or comparing recovery with NPB at 10, 20 or 30 min. However, at 20 min of NBP, pAVP was slightly lower than at prestudy (p less than 0.05). Central venous pressure (CVP) decreased significantly during NPB, and central transmural venous pressure (CVP-P) increased significantly from -0.9 +/- 0.8 mm Hg to 3.8 +/- 0.7, 4.3 +/- 0.7 and 4.5 +/- 0.6 mm Hg (p less than 0.001) after 10, 20 and 30 min, respectively. Systolic, diastolic and mean arterial pressure and heart rate did not change significantly during NPB. Diuresis, natriuresis, kaliuresis, osmotic excretion and clearance were slightly increased during the recovery hour after NPB compared to prestudy, while urine osmolality decreased during NPB (n = 6). However, none of these changes were significant. There was no significant correlation between CVP-P and pAVP. In conclusion, -10 mm Hg NPB for 30 min in upright sitting subjects did not change pAVP consistently, while CVP-P was significantly increased and HR and arterial pressures were unchanged. This lends support to the concept that arterial baroreceptors and not cardiopulmonary mechanoreceptors are of importance in regulating AVP secretion in man.