Colloid osmotic pressure of the subcapsular interstitial fluid of rat kidneys during hydropenia and volume expansion

Summary To determine the colloid osmotic pressure of subcapsular interstitial fluid in rat kidneys two different methods were used. Collection of subcapsular fluid with glass pipettes or implanted microcatheters and subsequent protein analysis resulted in a protein concentration of 1.8g%±0.6 and 2.0g%±0.8, respectively. Lymph protein concentration was not significantly different from that of subcapsular fluid samples. During extracellular volume expansion both subcapsular and lymph protein concentration fell to 0.42g%±0.23 and 0.7g%±0.5. Application of anin vivo oncometric method resulted in an effective oncotic pressure about twice that estimated from protein determinations. Using average values for intratubular and intracapillary oncotic and hydrostatic pressures a tubulo-interstitial net driving force of 20 mm Hg and an interstitial-capillary net driving force of 13 mm Hg is estimated in hydropenic animals. During volume expansion net transtubular pressure gradient is reduced to about 60–70% of control while the transcapillary gradient is virtually unchanged.     

On the role of the interstitial volume in the response of the rat to blood volume expansion

Patterns of body fluid distribution and selected cardiovascular and renal responses were studied following vascular expansion in normal rats and in rats with altered interstitial fluid volume produced by dehydration, prehydration or hyperoncotic albumin infusion. In all four groups the patterns of the renal excretory response and the accompanying change in central venous pressure (CVP) were closely parallel and the disturbance in CVP was finally corrected in the presence of a considerable residual vascular expansion. During the diuresis and saluresis following iso-oncotic vascular expansion in prehydrated and dehydrated rats, both groups removed fluid chiefly from the interstitium; this fluid removal was attributable mainly to urinary excretion in prehydrated rats but mainly to redistribution into the cellsin dehydrated rats. In the latter series, preferential renal excretion of sodium over water was observed. Hyperoncotic vascular expansion led to a peak renal excretory response only 70% of that following iso-oncotic expansion. The excreted volume was accounted for by a similar depletion of interstitial fluid after the iso-oncotic load. These findings are consistent with the hypothesis that the renal response to volume expansion regulates some parameter which is more closely related to the mean central venous pressure than to the vascular volume. This regulation was associated with incomplete correction of the vascular expansion and absolute decrease in interstitial fluid volume compared to the initial size of that compartment. This provides support for a functionally important influence of the interstitial volume on venous compliance.     

Hydrostatic and oncotic pressures in the interstitium of dehydrated and volume expanded rats

The pressures in the renal interstitial space seem to have important influence on the setting of the sensitivity of the tubuloglomerular feedback that controls the glomerular filtration rate (GFR), and on the rate of proximal tubular fluid reabsorption. Measurements were made of interstitial pressure conditions, GFR, renal plasma flow (RPF), urinary excretion of sodium and potassium, and plasma renin activities in dehydrated animals and normopenic controls, before and after saline volume expansion (5% of body weight and hour). Colloid osmotic pressure, estimated from the protein concentration in renal hilar lymph, was 7.5 mmHg in the dehydrated animals (controls 2.8 mmHg) and decreased to 3.1 (controls 1.7 mmHg) after volume expansion. The lymph flow rate was increased in both groups of animals after volume expansion. Interstitial hydrostatic pressure, measured in the subcapsular space, was 2–3 mmHg in dehydrated and control animals and increased to 3–4 mmHg after volume expansion. In dehydrated rats GFR and RPF was reduced to 60% of the control values, but after volume expansion they regained control values. After volume expansion, urinary excretion of fluid and electrolytes increased more in controls than in dehydrated rats. Plasma renin activity was dereased in both groups of rats after volume expansion. Thus, in dehydrated animals there was a high colloid osmotic pressure and a low hydrostatic pressure in the renal interstitium, while after volume expansion the oncotic pressure fell and the hydrostatic pressure rose. The effect of volume expansion was found to be dependent on the preceding volume balance situation in the animal.     

Model of interstitial pressure as a result of cyclical changes in the capillary wall fluid transport.

Reported interstitial pressures range from -8 to +6 mm Hg in different tissues and from <-20 mm Hg in burned tissue or more than +30 mm Hg in tumors. We have tried to link interstitial pressure to the here proposed cyclical changes in the fluid transport across the capillary wall.In the presented model interstitial pressure is considered as an average of pressures in numerous pericapillary spaces. A single pericapillary pressure is a dynamic difference between the net outward (hydraulic pressure+interstitial colloid osmotic pressure) and inward (plasma colloid oncotic pressure) forces. Hence, dominating net outward forces would result in a positive pericapillary interstitial pressure, while stronger inward forces would produce negative pressures in the pericapillary space. All interruptions of blood flow leave some blood in capillaries with a normal oncotic pressure and no hydrostatic pressure that might act as a strong absorber of interstitial fluid until the blood flow is reestablished.Model assumptions for the systemic circulation capillaries include (a) precapillary sphincters can almost entirely stop the capillary flow, (b) only a minority of sphincters are normally open in the tissue, and (c) hydrostatic pressures in unperfused capillaries are similar to the pressures at their venous ends.The key proposal is that capillaries with closed precapillary sphincters along their entire length have low hydrostatic pressure of 10 to 15 mm Hg. This pressure cannot force filtration, so these capillaries reabsorb interstitial fluid from the pericapillary space along their entire length. In the open capillaries, hydrostatic pressure filtrates fluid to the pericapillary space along most of their length. Fluid enters, moves some 20 or 30 micrometers away and back to be reabsorbed at the same point. Closed periods are periods of intense fluid reabsorption, while the short open periods refill the space with fresh fluid. It can be calculated that subcutaneous tissue interstitial pressure values might develop if the closed periods are 1.14 to 2.66 times longer than the open periods. Positive interstitial pressures observed in some organs might develop if open periods are longer than the closed periods.High interstitial colloid pressure in lungs makes both perfused and unperfused capillaries absorptive, resulting in more negative values of lung interstitial pressure. The same model is used to explain interstitial pressure values in tumors, burned tissue and intestinal villi.     

Acute saline expansion lowers blood pressure of early DOCA-salt hypertensive rats

Changes in blood pressure and body fluids volume caused by an acute saline load were studied in 6 normal and 7 DOCA-salt early hypertensive rats having normal inulin space and plasma volume. After loading, blood pressure increased in the normal group (+23 mm Hg) and fell (–17 mm Hg) in the DOCA-salt group. Expansion of extracellular fluid volume was similar in both groups but expansion of plasma volume was twice as high in the DOCA-salt than in the normal group. The results are compatible with an inhibition of a volume-sensitive vasopressor mechanism possibly involving vasopressin.     

The interstitial fluid content in working muscle modifies the cardiovascular response to exercise

Summary The volume of interstitial fluid in the limbs varies considerably, due to hydrostatic effects. As signals from working muscle, responsible for much of the cardiovascular drive, are assumed to be transmitted in this compartment, blood pressure and heart rate could be affected by local or systemic variations in interstitial hydration. Using a special calf ergometer, eight male subjects performed rhythmic aerobic plantar flexions in a supine position with dependent calves for periods of 7 min. During exercise heart rate, blood pressure, oxygen uptake (VO₂) and blood lactate concentrations were measured in two different tests, one before and after interstitial calf dehydration through limb elevation for 25 min, compared to the other, a control with unaltered fluid volume in a maintained working position. Impedance plethysmography showed calf volume to be stabilized in the control position. Leg elevation by passive hip flexion to 90° resulted in a fast (vascular) volume decrease lasting <2 min, followed by a slow linear fluid loss from the interstitial compartment. Then, when returned to the control position, adjustment of vascular volume was completed within 2 min and exercise could be performed with dehydration remaining in the interstitium only. Cadiovascular response was identical at the start of both tests. However, exercising with dehydrated calves elicited a significantly larger increase in heart rate compared to the control, whereasVO₂ was identical. The blood pressure response was shown to be only slightly enhanced. Structural interstitial features varying with hydration, most likely chemical or mechanical ones, may have been responsible for this amplification of signals.     

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

Summary 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<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<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.This investigation was supported by the Danish Space Board grant no. 1112-13/84, 1112-19/84, 1112-33/84, and 1112-34/84     

Effect of elevated interstitial pressure on the renal cortical hemodynamics.

The influence of renal interstitial pressure on the resistance pattern within the superficial cortical vasculature has been investigated from determinations of 1) the glomerular blood flow eith a modified microsphere technique and 2) the intravascular hydrostatic pressures. Interstitial pressure was monitored via a 50 mum PVC-catheter placed into the subcapsular interstitial space. Two conditions were analyzed viz. a) elevation of uretheral pressure to 20 mm Hg and b) venous stasis to 10-15 mm Hg. Both conditions produced an increase in the interstitial pressure from 1-2 mm Hg to about 5 mm Hg as well as an increased hilar lymph flow and protein flow of about the same size. The vascular reactions were different, however. Uretheral stasis (but not the stasis of a single nephron) produced a decreased resistance in the afferent arteriolae with a concomitant increae in the pressures in the glomerular capillaries, and the peritobular capillary network. In contrast, venous stasis produced only small changes in the parameters studied but for the obvious rise in the peritubular capillary pressure. The results suggest that factors other than the interstitial pressure are governing the afferent vascular tone; the tubular wall tension might be one of these factors.     

Effect of Elevated Interstitial Pressure on the Renal Cortical Hemodynamics

The influence of renal interstitial pressure on the resistance pattern within the superficial cortical vasculature has been investigated from determinations of I) the glomerular blood flow with a modified microsphere technique and 2) the intravascular hydrostatic pressures. Interstitial pressure was monitored via a 50 μm PVC-catheter placed into the subcapsular interstitial space. Two conditions were analyzed viz. a) elevation of iiretheral pressure to 20 mm Hg and b) venous stasis to 10–15 mm Hg. Both conditions produced an increase in the interstitial pressure from 1–2 mm Hg to about 5 mm Hg as well as an increased hilar lymph flow and protein flow of about the Same size. The vascular reactions were different, however. Urethcral stasis (but not the stasis of a single nephron) produced a decreased resistance in the afferent arteriolae with a concomitant increase in the pressures in the glomerular capillaries, and the peritubular capillary network. In contrast, venous stasis produced only small changes in the parameters studied but for the obvious rise in the peritubular capillary pressure. The results suggest that factors other than the interstitial pressure are governing the afferent vascular tone; the tubular wall tension might he one of these factors.     

The distensibility of mesenteric venous microvessels

Summary In 20 experiments the distensibility characteristics of venous microvessels of 22–148 m internal diameter in response to arterial and venous pressure changes were examined microphotographically in the isolated and perfused mesentery of the dog. Over a range of arterial pressure between 0 and 170 mm Hg venular diameter changed by 31,8±8,8% and venular length by 6.3±4.4%. Venular length changes were significantly correlated to corresponding changes in the accompanying arterioles, whereas no correlation could be found between changes of length and diameter and the control diameters. With venous pressure elevation from 0 to 30 mm Hg an increase of the volume of venous microvessels of about 360% was measured; beyond a venous pressure of 30 mm Hg a limitation of distensibility was observed in these vessels. The moduli of volume elasticity calculated from these data were lower than the moduli reported for the total venous vasculature of the intestinal bed in the range of physiological pressures. It is concluded that the venous microvessels represent the most distensible elements of the venous vascular system.     

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

Summary 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±4.1mm Hg (N=4, p<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<0.02). In connection with the injection, SAP increased from 128.5±4.2 mm Hg to 134.3±5.4 mm Hg (N=6, p<0.025), PP from 56.5+-2.8 mm Hg to 62.7±3.5 mm Hg (N=6, p<0.01), HR from 54.0±3.1min^–1 to 59.2±4.1 min^–1 (N=6, p<0.01), and LVETI from 407.0±5.6 ms to 413.1±6.0 ms (N=6, p<0.02). This study suggests that endorphins do not have a significant action on the cardiovascular system in the compensated stage of hypovolaemic shock in humans. We found, however, weak evidence that naloxone increases SAP, HR, and LVETI during rest.     

Hydrostatic pressures within the vascular structures of the rat kidney

Summary The pressure conditions at the distal end of the interlobular arteries and in the interlobular veins were investigated from the pressures obtained in superficial small arteries and veins, accidentally found on the kidney surface, during the subsequent blockade of the blood stream in the down-stream and up-stream direction, respectively.The results suggested a hydrostatic pressure in the distal end of the interlobular arteries of about 85 mm Hg under normotensive conditions-a pressure which remained fairly constant when the perfusion pressure in the renal artery was decreased within the autoregulation range. The results indicate a considerable pressure drop of about 40 mm Hg along the interlobular arteries. During hypotension this pressure drop decreased, implying a decreased resistance in the interlobular arteries, i.e.a typical autoregulative response.The pressure in the interlobular veins amounted to about 5 mm Hg, which is a few mm Hg higher than that in the renal vein and about 7 mm lower than that in the peritubular capillary network. The results suggest a flow resistance located somewhere between the peritubular capillaries and the intrarenal veins. This resistance is not influenced by vasoactive substances but it is decreased when the systemic venous pressure is raised above 10 mm Hg. The resistance seems to act in the direction of protecting the peritubular capillaries from minor changes in the central venous pressure.     

Correlation between luminal hydrostatic pressure and proximal tubular fluid reabsorption in the rat kidney

Summary Split-drop experiments were performed to evaluate the effect of changes in luminal hydrostatic pressure on net fluid reabsorption in proximal convoluted tubules of the rat kidney. While hydrostatic pressure in control droplets averaged 28.9±1.03 mm Hg, it increased to a mean of 65.2±3.3 mm Hg during pressure elevation and fell to 10.8±1.04 mm Hg during pressure reduction. In paired measurements in identical tubules net fluid absorption changed from a control value of 2.96±0.14 nl/min·mm to 3.88±0.14 nl/min·mm when luminal pressure was elevated. During pressure reduction net fluid absorption fell from a control of 2.98±0.09 nl/min·mm to 2.26±0.13 nl/min·mm (P<0.001). This dependency of fluid absorption upon hydrostatic pressure was not greatly affected by the finding that microphotography overestimated the true intradroplet volume by 31% during control and by 30.2% and 50% during elevated and reduced pressure respectively. From the relation between the changes of net absorption and luminal hydrostatic pressure an apparent hydraulic conductance of 0.04 nl/min·mm Hg was estimated.     

Changes of peripheral venous tone and central transmural venous pressure during immersion in a thermo-neutral bath

Summary Peripheral venous tone, central venous and oesophageal pressures were recorded while the upright sitting subjects were immersed to the neck in a thermoneutral water bath. The central venous pressure rose from 3.4 to 15.2 mm Hg and the oesophageal pressure from –0.4 to +3.4 mm Hg. The transmural pressure, which determines the enddiastolic volume of the heart, increased by 8.0 mm Hg. Plethysmographic determinations of peripheral venous tone revealed a relaxation of the peripheral veins: after a quick initial decrease of the volume elasticity coefficient (E₁₅) from 16.6 to 13.5 mm Hg/ml/100 g tissue there is a continuous decline to 11.8 mm Hg/ml/100 g tissue after 3 hrs immersion. This relaxation persists for at least 1 hr after termination of immersion.This work was supported by Contract No. F44620-71-C-0117 of the Air Force Office of Scientific Research (OAR), European Office of Aerospace Research.with the technical assistance of H. Dannenberg     

Redistribution of cardiac output after hypothalamic lesions and hemorrhage

Summary The effects of ablation of the anteroventral portion of the third cerebral ventricle (AV3V) on cardiac output and distribution of regional blood flows were determined in conscious rats using 15 m radiolabelled microspheres before, and 2 min and 15 min after hemorrhage (n=11 for each group). Prior to hemorrhage, cerebral blood flow was significantly greater (216±30 ml/min/100 g), and cerebral vascular resistance was lower (0.60±0.09 mm Hg/ml/min/ 100 g) in rats with AV3V lesions than in controloperated animals (132 ±16 ml/min/100 g; 0.92+0.1 mm Hg/ml/min/100 g, respectively), while mean arterial blood pressure, cardiac output, and regional blood flow to other organs were similar. Less blood was withdrawn from animals with AV3V lesions (4.4 ±0.6 ml) than from control-operated rats (6.0±0.5 ml) to reduce blood pressure to approximately 65 mm Hg. Hemorrhage decreased cerebral vascular resistance in control-operated animals (0.52±0.07 mm Hg/ml/min/100 g), but not in rats with AV3V lesions (0.48±0.1 mm Hg/ml/min/100 g). Cardiac output and regional blood flow to other organs were similar between rats with AV3V lesions and controloperated animals following hemorrhage. These data demonstrate that electrolytic ablation of the AV3V region results in a selective increase in cerebral blood flow and decreased cerebral vascular resistance, but does not alter the reflex changes in regional blood flow evoked by hemorrhage.     

Measurement of interstitial fluid pressure: Comparison of methods

Interstitial fluid pressure (IFP), i.e., the pressure in a saline-filled tube brought into contact with the interstitium, has been measured in cats with two “acute” [micropipettes and wick-in-needle (WIN)] and two chronic (perforated and porous capsules) methods. In a control situation, similar pressures of −1.5 and −1.6 mm Hg were recorded in skin with micropipettes and both types of capsules, respectively, while WIN pressure in subcutis was −1.2 mm Hg. IFP in skeletal muscle was −0.5, −0.5, and −1.1 mm Hg as recorded with micropipettes, WIN, and porous capsules, respectively. During infusion of Ringer's solution, pressures in both types of capsules rose by 4 to 6 mm Hg, while pressure recorded with the acute methods increased by 1 to 1.5 mm Hg only. Two hours after infusion all techniques gave similar pressures. Peritoneal dialysis for 2 hours reduced micropipette and WIN pressures by 3 to 4 mm Hg. Pressure in perforated capsules fell by 10 mm Hg during dialysis and remained low for an additional 2 hours, while porous capsule pressure fell by 7 mm Hg during dialysis but thereafter increased and reached the pressure recorded with micropipettes and WIN 2 hours after ended dialysis. In both overhydration and dehydration, capsules probably react to changes in interstitial fluid colloid osmotic pressure; in overhydration the capsules react also to changes in capillary pressure, resulting in the discrepancy between chronic and acute methods during non-steady-state conditions. In conclusion, acute and chronic methods record similar pressures during steady-state conditions, but the chronic methods are sensitive to changes in vascular pressure and interstitial fluid colloid osmotic pressure and are therefore not suitable for measuring the changes that occur in IFP within a few hours.     

Estimation of parameters in transcapillary fluid movement by digital simulation

A modified computer model of the terminal vascular bed is presented. The capillary model consists of two parts; the arterial and venous capillary segments in series with the corresponding resistances. A third segment, in parallel with the capillary, represents the varying volume interstitial space. In addition to equations describing the fluid flow between the various segments, the dynamics of protein-mass flow are described. In contrast to models described by earlier investigators, the plasma osmotic pressure π_PL is also a variable. Thus, small changes in π_PL due to variations in venous pressure could be detected. The percentage increase in π_PL per mm Hg increase in venous pressure has an average value of 0·255% per mm Hg. Finally, a hysteresis phenomenon was demonstrated while increaseing and decreasing extravascular tissue volume; the total simulated energy expenditure was EH=1·542 mm Hgx ml for a venous pressure change from 5 to 20 mm Hg. An abbreviated report was presented at the 3rd Annual Meeting of the Biomedical Engineering Society, 7th April, Baltimore, Md., USA     

On the edema-preventing effect of the calf muscle pump

Summary During motionless standing an increased hydrostatic pressure leads to increased transcapillary fluid filtration into the interstitial space of the tissues of the lower extremities. The resulting changes in calf volume were measured using a mercury-in-silastic strain gauge. Following a change in body posture from lying to standing or sitting a two-stage change in calf volume was observed. A fast initial filling of the capacitance vessels was followed by a slow but continuous increase in calf volume during motionless standing and sitting with the legs dependent passively. The mean rates of this slow increase were about 0.17%·min⁻¹ during standing and 0.12%·min⁻¹ during sitting, respectively. During cycle ergometer exercise the plethysmographic recordings were highly influenced by movement artifacts. These artifacts, however, were removed from the recordings by low-pass filtering. As a result the slow volume changes, i.e. changes of the extravascular fluid were selected from the recorded signal. Contrary to the increases during standing and sitting the calf volumes of all 30 subjects decreased during cycle ergometer exercise. The mean decrease during 18 min of cycling (2–20 min) was −1.6% at 50 W work load and −1.9% at 100 W, respectively. This difference was statistically significant (p≤0.01). The factors which may counteract the development of an interstitial edema, even during quiet standing and sitting, are discussed in detail. During cycling, however, three factors are most likely to contribute to the observed reduction in calf volume: (1) The decrease in venous pressure, which in turn reduces the effective filtration pressure. (2) An increased lymph flow, which removes fluid and osmotically active colloid proteins from the interstitial space. (3) An increase in muscle tissue pressure, which counteracts the intravascular pressure during the muscle contraction thus playing an important role as an edema-preventing factor, which has not been considered to date.     

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

Summary To quantify the effect of 60 mm Hg lower-body positive pressure (LBPP) on orthostatic blood-volume shifts, the mass densities (±0.1 g· l^–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°) 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 · l^–1, and by 0.8±0.2 g · l^–1 (±SD) (N=9), respectively. In the subsequent period of tilt without LBPP, BD and PD increased further to +3.6±0.9 g · l^–1, and to +2.0±0.7 g · l^–1 (N=7) compared to supine control. The density increases in both periods were significant (p<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 · l^–1,N=9), and for subsequent tilt after deflation (1002.8±4.1 g · l^–1,N=7) were different from each other (p<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<0.01), and 3.5±2.1% (p<0.05), respectively. Thus, about half of the postural hemoconcentration occurring during passive head-up tilt was prevented by application of 60 mm Hg LBPP.H. Hinghofer-Szalkay was a European Space Agency fellow on leave from the Physiological Institute, Karl-Franzens-University, A-8010 Graz, Austria.     

Effects of atrial natriuretic peptide (ANP) on jejunal net fluid absorption in the rat

The role of atrial natriuretic peptide (ANP) on jejunal net fluid transport was studied in intact rats as well as in rats subjected to a perivascular denervation of the intestinal segment. In rats with intact nerves, an acute volume expansion with 5% albumin (10% of estimated blood volume) decreased jejunal net fluid absorption by approximately 70% compared to control animals not subjected to volume expansion. After a perivascular denervation of the intestinal segment, the acute volume expansion reversed net fluid absorption into a net fluid secretion. In order to reduce the volume expansion-induced endogenous release of ANP, one group of rats was subjected to a right atrial appendectomy 7 days prior to the experiments. In these animals, the intestinal response to the same 10% volume load was blunted compared to controls. Administration of rat alpha-ANP (99-126; 5 micrograms kg-1 i.v.) induced effects similar to those of volume expansion both in rats with intact perivascular nerves as well as in denervated animals. Volume expansion increased mean arterial pressure (MAP) as well as central venous pressure and decreased heart rate (HR) in all groups. When exogenous ANP was administered, a fall in MAP was seen, while HR remained unchanged. In conclusion, these data strongly indicate a physiological role for ANP in jejunal fluid transfer in response to acute volume expansion.