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.     

Oncotic pressures opposing filtration across non-fenestrated rat microvessels

We hypothesized that ultrafiltrate crossing the luminal endothelial glycocalyx through infrequent discontinuities (gaps) in the tight junction (TJ) strand of endothelial clefts reduces albumin diffusive flux from tissue into the 'protected region' of the cleft on the luminal side of the TJ. Thus, the effective oncotic pressure difference (σπ) opposing filtration is greater than that measured between lumen and interstitial fluid. To test this we measured σπ across rat mesenteric microvessels perfused with albumin (50 mg ml⁻¹) with and without interstitial albumin at the same concentration within a few micrometres of the endothelium as demonstrated by confocal microscopy. We found σπ was near 70% of luminal oncotic pressure when the tissue concentration equalled that in the lumen. We determined size and frequency of TJ strand gaps in endothelial clefts using serial section electron microscopy. We found nine gaps in the reconstructed clefts having mean spacing of 3.59 μm and mean length of 315 nm. The mean depth of the TJ strand near gaps was 67 nm and the mean cleft path length from lumen to interstitium was 411 nm. With these parameters our three-dimensional hydrodynamic model confirmed that fluid velocity was high at gaps in the TJ strand so that even at relatively low hydraulic pressures the albumin concentration on the tissue side of the glycocalyx was significantly lower than in the interstitium. The results conform to the hypothesis that colloid osmotic forces opposing filtration across non-fenestrated continuous capillaries are developed across the endothelial glycocalyx and that the oncotic pressure of interstitial fluid does not directly determine fluid balance across microvascular endothelium.     

Kinetics of the Glomerular Ultrafiltration in the Rat Kidney. A Theoretical Study

The glomerular filtration process was evaluated theoretically from micropuncture data obtained from Sprague-Dawley rats. The hydrostatic pressures in the glomerular capillaries and Bowman's space minus the oncotic pressure in systemic plasma gave the net driving force at the proximal end of the glomerular capillary. From the single nephron filtration fraction the mean net driving force over the glomerular membrane was calculated to be 20 mm Hg during normotension, decreasing to 12 mm Hg during a perfusion pressure of 80 mm Hg. The hydraulic permeability for one glomerulus was 0.7-0.8 nl/min. 100g b. wt. mmHg. The pressures at the distal end of the glomerular capillaries were 13 and 6 mm Hg under the above two conditions, indicating non-equilibrium of the filtration process at the end of the glomerular capillary. It was shown that the glomerular filtration rate is mainly influenced by the driving pressures. During hypotension an increased plasma flow dependency was evident. Brenner et al. found a filtration equilibrium and a plasma flow dependent glomerular filtration rate in a mutant Wistar rat strain. The discrepancy between their results and ours is due to the low glomerular plasma flow and hydrostatic pressures in the Wistar rats. It is concluded from our results that both pre- and postglomerular resistances may influence the glomerular filtration rate and glomerular plasma flow independently.     

Kinetics of the glomerular ultrafiltration in the rat kidney. A theoretical study.

The glomerular filtration process was evaluated theoretically from micropuncture data obtained from Sprague-Dawley rats. The hydrostatic pressures in the glomerular capillaries and Bowman's space minus the oncotic pressure in systemic plasma gave the net driving force at the proximal end of the glomerular capillary. From the single nephron filtration fraction the mean net driving force over the glomerular membrane was calculated to be 20 mm Hg during normotension, decreasing to 12 mm Hg during a perfusion pressure of 80 mm Hg. The hydraulic permeability for one glomerulus was 0.7-0.8 nl/min-100 g b.wt. mmHg. The pressures at the distal end of the glomerular capillaries were 13 and 6 mm Hg under the above two conditions, indicating non-equilibrium of the filtration process at the end of the glomerular capillary. It was shown that the glomerular filtration rate is mainly influenced by the driving pressures. During hypotension an increased plasma flow dependency was evident. Brenner et al. found a filtration equilibrium and a plasma flow dependent glomerular filtration rate in a mutant Wistar rat strain. The discrepancy between their results and ours is due to the low glomerular plasma flow and hydrostatic pressures in the Wistar rats. It is concluded from our results that both pre- and postglomerular resistances may influence the glomerular filtration rate and glomerular plasma flow independently.     

Fluid transfer from skeletal muscle to blood during hemorrhage Importance of beta adrenergic vascular mechanisms

Vascular reactions in the cat lower leg muscles in response to short-term (10 min) hemorrhagic hypotension (?80 mmHg) were studied before and after regional blockade of the β-adrenoceptors. In the muscle region with intact β-adrenoceptors, hemorrhage raised vascular resistance by about 80% and caused a dilatation of the precapillary sphincters, the latter effect evidenced in terms of a 35% increase of the capillary filtration coefficient. Concomitantly, an absorption of extravascular fluid to the blood stream occurred, a process tending to compensate for the reduction of intravascular fluid volume. After regional β-blockade there was quite a marked augmentation of the hemorrhage induced increase of vascular resistance whereas the inhibition of precapillary sphincter tone and the transcapillary fluid absorption were almost abolished. These observations indicate that bleeding is associated with a significant β-adrenergic dilator influence in both the resistance vessels and precapillary sphincters of skeletal muscle and that the β-dilator mechanism may be essential for the important, compensatory fluid gain from the extravascular to the intravascular space during hemorrhage. The observed β-adrenergic mediation of the net transcapillary fluid absorption could be ascribed to resetting of the pre-/postcapillary resistance ratio, leading to decreased capillary hydrostatic pressure, and to the dilator influence in the precapillary sphincters, leading to an increased number of the patent capillaries available for the transcapillary fluid exchange.     

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.     

Peritubular capillary control of proximal tubule reabsorption in the rat.

Changes in peritubular capillary hydrostatic and oncotic pressures, which probably affect net interstitial pressure and, thus, the force on fluid movement across the tubule basement membrane, can modulate absolute proximal reabsorption rate (APR). To examine the relationship between APR and net interstitial pressure, we measured peritubular capillary hydrostatic and oncotic pressure, single nephron filtration rate, APR, absolute distal reabsorption (ADR), and tubular hydrostatic pressure in hydropenic, saline-loaded, and plasma-loaded rats. Net interstitial pressure in saline loading was estimated from subcapsular hydrostatic pressure and lymph protein concentration measurements. The surface area-hydraulic conductivity product of the peritubular capillary network was estimated from these measurements with a model of capillary fluid exchange in which fluid uptake was defined to be APR plus ADR. The estimated value was assumed to remain constant in all three states, and was then used to estimate net interstitial pressure in hydropenic and plasma-loaded rats. APR and net interstitial pressure correlated strongly, a finding consistent with the hypothesized role for net interstitial pressure in regulating proximal reabsorption.     

Targeted O2 delivery by low-p50 hemoglobin: a new basis for hemoglobin-based oxygen carriers

We have proposed new criteria for a successful cell-free, hemoglobin-based O2 carrier. These include increased molecular radius, increased viscosity, increased oncotic pressure, and reduced p50. A new molecule, MalPEG-Hb, formulated at 4.2g/dL in lactated Ringer's solution (MP4), has been produced according to these new criteria. MP4 has a p50 of 5-6 mm Hg, oncotic pressure of 49mm Hg and viscosity of 2.2cPs. After 50% exchange transfusion with MP4, rats survive a 60% controlled hemorrhage in spite of total hemoglobin of 7.8 g/dL and plasma hemoglobin concentration of 1.6 g/dL. This model results in 50% mortality in control animals and 100% mortality in animals exchange-transfused with either crosslinked or polymerized hemoglobin. Oxygen supply to tissue was measured directly in the hamster skinfold model, in which O2 release in precapillary and capillary vessels can be quantified. The data demonstrate that the effectiveness of MP4 results from its ability to conserve O2 in precapillary vessels and release O2 in capillaries, thereby "targeting" O2 to hypoxic tissue. Preservation of functional capillary density and prevention of vasoconstriction further contribute to the effectiveness of this new formulation.     

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.     

An analysis of interstitial fluid pressure in the web of the bat wing.

A mathematical theory of interstitial fluid motion and capillary exchange is developed in order to understand and explain measurements of capillary and interstitial fluid pressure in the bat wing, in which a high degree of vasomotor activity occurs. As a result of precapillary sphincter activity, fluid is alternately filtered and reabsorbed from the capillary, and previous studies of related steady problems by the author suggest that the interstitial fluid pressure should oscillate with time. Wiederhielm and Weston did not observe such fluctuations when they measured tissue pressures near the capillaries. This apparent paradox is resolved in the present paper by including unsteady effects. It is shown that pressure oscillations are predicted, but because of the very high vasomotor frequency they die out within a very short distance from the capillary wall. The capillary pressure measurements of Wiederhielm and Weston are also explained in terms of precapillary sphincter activity.     

Intratubular and peritubular capillary hydrostatic and oncotic pressures after chronic renal sympathectomy in the anaesthetized rat

The possible role of peritubular capillary physical forces in the diuretic-natriuretic effects of chronic renal denervation was investigated in Inactin-anaesthetized non-diuretic control (C) and unilaterally denervated (D) rats. Micropuncture techniques were combined with measurement of intratubular and peritubular capillary hydrostatic pressures and afferent and efferent arteriolar plasma oncotic pressures were determined, as well. Compared to data of C rats and of innervated kidneys, marked denervation diuresis and natriuresis were seen without changes in GFR. Both late proximal and early distal (F/P)_In values were significantly lower in D kidneys with similar SNGFR. Afferent (π_a) and efferent (π_e) arteriolar oncotic pressures were unchanged by denervation (C-π_a = 23.3 ± 0.79, π_e = 29.9 ± 0.87 mm Hg; D-π_a = 23.2 ± 0.94, π_e = 29.8 ± 1.04 mm Hg). Proximal intratubular hydrostatic pressure was moderately but significantly higher in D kidneys (C=11.9±0.5, D=13.7±0.3 mm Hg,P<0.01), while peritubular capillary pressures were: efferent arteriole (C=13.9±0.5, D=13.4±0.6 mm Hg, NS). It is concluded that the tubular effects of chronic renal sympathectomy are not dependent on changes in Starling forces of the peritubular environment.     

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.     

Pressure in the glomerular capillaries of the rat kidney and its relation to arterial blood pressure

Summary The pressure in the glomerular capillaries of the rat kidney was determined by micropuncture of individual nephrons. The proximal tubule was blocked by injection of viscous oil. The intratubular hydrostatic pressure increased until it reached a steady state, the intratubular stop-flow pressure. Since the glomerular capillary wall is an ultrafiltration membrane, impermeable to proteins, the sum of intratubular stop-flow pressure plus the plasma colloid osmotic pressure should equal the pressure in the glomerular capillaries. This pressure increased as the arterial pressure was raised from 60 to 90 mm Hg. Thereafter it remained constant at 88±4 mm Hg despite further elevation of the arterial pressure up to 160 mm Hg. Determination of the stop-flow pressure in Bowman's capsule and in the proximal tubules of denervated kidneys gave the same results as above.The hydrostatic pressure drop in the afferent arterioles was determined by subtracting the glomerular capillary pressure from the arterial pressure. This pressure drop was negligible at arterial pressures below 90 mm Hg and increased linearly as the arterial pressure was elevated from 90 to 160 mm Hg.Both the above findings are compatible with and confirm the principle of autoregulation of renal blood flow and glomerular filtration rate.Supported by NIH Grant Nr. AM 06806-03 and by Deutsche Forschungsgemeinschaft.From the Dept. of Pediatrics, University of Wisconsin, Madison, Wisconsin, U.S.A. Supported by the National Cystic Fibrosis Foundation.     

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.     

Modulation of proximal tubular hydraulic conductivity by peritubular capillary oncotic pressure

Fluid absorption from the proximal tubular lumen is probably a multifactorial process. Earlier studies from our laboratory have indicated that a transepithelial hydrostatic and oncotic pressure difference may be the driving force for as much as 30% of the reabsorbed fluid. During saline volume expansion proximal tubular reabsorption declines and the present experiments were undertaken to investigate whether this reduction could be caused by changes in the passively driven flux component. The hydraulic conductivity was therefore determined from the reabsorptive rate in split oil droplets with normal and high hydrostatic pressure gradients across the wall, at the same time as the peritubular capillary net-work was perfused with solutions containing a colloid of high or low concentration. In the reabsorption experiments the split oil droplet radius was measured and in a separate series of experiments the relationship between droplet radius and pressure was determined; this was found to be 7.3 mmHg pressure increase per 1 μm increase in radius. The increase in the rate of reabsorption from the droplets due to increased intraluminal hydrostatic pressure was 1.02±0.13 nl/min/mm tubular length when a solution with a high colloid concentration was perfused through the capillary net-work, compared with 0.41=0.11 nl/min/mm tubular length when a low colloid containing solution was used for perfusion. The hydraulic conductance in the proximal tubular wall at high colloid perfusion was calculated to be 0.54 nl/min mm mmHg while at a low capillary colloid oncotic pressure it was significantly lower 0.025 nl/min mm mmHg. This drop in hydraulic conductance might be one factor responsible for the decline in fluid absorption in animals exposed to saline volume expansion.     

Changes in interstitial pressure during and after blood volume expansion in rats

Summary Interstitial fluid pressure was measured via a chronically implanted capsule before, during and after acute isotonic, iso-oncotic blood volume expansion in normal or in 48-h dehydrated rats. At the same time, the patterns of body fluid distribution, of selected renal responses and of mean arterial and mean central venous pressure responses were studied. Dry tissue weight (DTW) was subsequently determined by freeze drying of the shaved carcass.Dehydration decreased plasma volume and interstitial fluid volume significantly below normal values. The initial intracapsular pressure in dehydrated animals (–3.7±0.6 mm Hg) was not significantly different from that in normal rats (–2.5±0.5), but dehydrated rats showed initially a very significantly lower effective interstitial compliance (0.0005 ml/mm Hg per gram DTW) than did the normal group (0.0704).In the course of the renal response to the volume load, effective interstitial complicance increased to 0.0350 in dehydrated rats but showed no change in normal rats. Neither group completely corrected its elevated blood volume; both returned their central venous pressures to pre-infusion levels; both decreased their interstitial fluid volumes below preinfusion levels and both decreased their intracapsular fluid pressures 1 mm Hg below the level prevailing in non-infused animals at that time.It is concluded that a reduction in interstitial, hydrostatic pressure can be a functionally important influence in the apparent control of central venous pressure following acute blood volume expansion.This study was supported by the Canadian Heart Foundation.     

Mechanics of lung fluid balance

Recent research in pulmonary physiology, anatomy, and mechanics have clarified our general understanding of liquid and solute transport through the lung. Fluid crosses the microvascular endothelial membrane at a rate that depends on gradients in the transmembrane hydrostatic and osmotic pressures and the conductance of the permeable membrane. Under normal conditions, the filtered fluid is removed by an efficient lymphatic pump. Edema accumulates in the lung when an increased flux due to an elevated vascular pressure or to a more permeable membrane is not matched by an adequate lymph clearance rate. Initially a favorable hydrostatic pressure gradient drives the excess fluid into interstitial spaces surrounding large blood vessels and airways away from filtration sites near capillaries and thereby ensures efficient gas exchange. Further edema formation reduces the pressure gradient, eventually leading to the flooding of alveolar air spaces and impaired gas exchange. I will focus on the role of the above forces in the regulation of extravascular lung water. It will become clear that many details of the general scheme are not known, and our conceptual understanding of the relevant mechanisms involved is often rudimentary and incomplete. Some of the more important questions pertain to the interstitial pressure around capillaries, the resistance and compliance of the interstitial matrix, and the role of the lymphatics in regulating interstitial fluid volume and interstitial pressure.     

Fluid transfer from skeletal muscle to blood during hemorrhage. Importance of beta adrenergic vascular mechanisms.

Vascular reactions in the cat lower leg in response to short-term (10 min) hemorrhagic hypotension (approximately 80 mmHg) were studied before and after regional blockade of the beta-adrenoceptors. In the muscle region with intact beta-adrenoceptors, hemorrhage raised vascular resistance by about 80% and caused a dilatation of the precapillary sphincters, the latter effect evidenced in terms of a 35% increase of the capillary filtration coefficient. Concomitantly, an absorption of extravascular fluid to the blood stream occurred, a process tending to compensate for the reduction of intravascular fluid volume. After regional beta-blockade there was quite a marked augmentation of the hemorrhage induced increase of vascular resistance whereas the inhibition of precapillary sphincter tone and the transcapillary fluid absorption were almost abolished. These observations indicate that bleeding is associated with a significant beta-adrenergic dilator influence in both the resistance vessels and precapillary sphincters of skeletal muscle and that the beta-dilator mechanism may be essential for the important, compensatory fluid gain from the extravascular to the intravascular space during hemorrhage. The observed beta-adrenergic mediation of the net transcapillary fluid absorption could be ascribed to resetting of the pre-/postcapillary resistance ratio, leading to decreased capillary hydrostatic pressure, and to the dilator influence in the precapillary sphincters, leading to an increased number of the patent capillaries available for the transcapillary fluid exchange.     

Die Filtrationsdrucke in der Arterienwand

Zusammenfassung Das Endothel und das faserarme subendotheliale Bindegewebe normaler Arterien haben vorwiegend plastisch-viscöse Eigenschaften und nehmen im Vergleich zur Lamina elastica interna und der faserreichen Media nur wenig elastische Spannung auf. Der intramurale Kompressionsdruck im subendothelialen Bindegewebe ist deshalb fast ebenso hoch wie der intravasale Druck.Die semipermeable Membran des Endothels trennt somit zwei Räume voneinander, den Blutraum und den Intimaraum, in welchem ein fast gleich hoher hydrostatischer Druck herrscht. Der kolloid-osmotische Druck des Blutes beträgt 25 mm Hg, der des subendothelialen Bindegewebes 2–3 mm Hg. Infolge der Differenz der kolloidosmotischen Drucke muß am Endothel der Arterien ein effektives Filtrationsgefälle von etwa 20 mm Hg wirksam werden, das im Gegensatz zu den Capillaren nicht von innen nach außen, sondern von außen nach innen gerichtet ist, also von der Intima zum Blut.

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Filtration Pressure in the Arterial Wall

Summary The physical properties of the endothelium and the subendothelial connective tissue of normal arteries are more plastico-viscous than elastic because the collagen and elastic fibers are thin and sparse in the ground substance of the normal intima.—Therefore, the elastic tension in the intima must be low while the intramural compression pressure in this layer approximately equals the intravascular pressure. The semipermeable membrane of the endothelium separates the blood from the subendothelial connective tissue. Both have nearly the same hydrostatic pressure.—The colloid osmotic pressure corresponds to 25 mm Hg in the blood and only to 2–3 mm Hg in the subendothelial connective tissue. This difference between the colloid osmotic and hydrostatic pressures generates an effective filtration pressure in the intima of approximately 20 mm Hg. In contrast to the capillaries, the gradient of the filtration pressure is not directed from inside to outside, but from outside to inside, which means from the intima to the blood.

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Als Diskussionsbemerkung in gekürzter Form vorgetragen auf Workshop-Conference, Fundamental data on reactions of vascular tissue in man. April 1970, Bad Schachen-Lindau.     

The Effects of Vasoconstrictor Fibre Stimulation on the Consecutive Vascular Sections of the Small Intestine of the Cat during Prolonged Regional Hypotension

A plethysmographic technique was used on the cat to investigate the effects of electrical stimulation of the regional sympathetic vasoconstrictor fibres on intestinal consecutive vascular sections during prolonged hypotension at approximately 55 or 30 mm Hg produced by graded arterial occlusion. The initial peak resistance and the capacitance responses declined continuously throughout the hypotensive period, the rate of decline being higher the lower the per-fusion pressure. After 2.5 h hypotension at 30 mm Hg the nervous vasoconstrictor effects on the resistance and capacitance vessels amounted to 50 and 30 per cent of control, respectively. The reactivity of the precapillary sphincters as reflected in the capillary filtration coefficient (CFC), was largely unaltered during the hypotension at the 55 mm Hg level. At the lower perfusion pressure a marked increase of CFC was noted between and during nervous stimulations. Mean capillary hydrostatic pressure was not significantly changed by nervous activation, hut seemed to increase in the latter half of most experiments at 30 mm Hg. When releasing the arterial clamp after a 30 mm Hg hypotension the whole cardiovascular system seemed to derange progressively. Mucosal ulcerations and bleedings were regularly found in all these animals.