Interstitial Fluid Colloid Osmotic Pressure Research Articles

Transcapillary forces in patients with lower limb ischemia

Starling pressures (interstitial fluid pressure, plasma and interstitial fluid colloid osmotic pressures) were measured in subcutaneous tissue at the ankle in 20 healthy controls and 27 patients with lower limb atherosclerosis. Subcutaneous interstitial fluid pressure (Pif) of the leg was also measured in seven patients with arterial emboli of the lower limb. Interstitial fluid was collected by implantation of nylon wicks and Pif was measured by the 'wick-in-needle', technique. The calculated reabsorption pressure (equal to capillary pressure if no net filtration occurs) was 18.3 mmHg in the group with atherosclerosis, which was higher than in controls (15.8 mmHg, P less than 0.05). Colloid osmotic pressure of interstitial fluid (COPif) was significantly lower in patients with atherosclerosis than in controls (5.9 v. 9.2 mmHg). This finding in itself could make those patients more susceptible to edema formation postoperatively. On the other hand, there was no correlation between COPif and ankle systolic blood pressure within the group of patients. There was a slight, but statistically significant positive correlation between ankle systolic blood pressure and Pif in patients with lower limb atherosclerosis although mean Pif was not different from controls (-1.0 v. -0.8 mmHg). In patients with arterial emboli, however, Pif was lower (mean -4.5 mmHg).

Interstitial fluid colloid osmotic and hydrostatic pressures in subcutaneous tissue of patients with nephrotic syndrome

Colloid osmotic pressure in plasma (IIp) and in interstitial fluid from subcutaneous tissue (IIi) was measured in 13 patients with nephrotic syndrome and in 20 healthy volunteers. Interstitial fluid was sampled by nylon wicks, and interstitial fluid pressure was measured by the 'wick-in-needle' technique. In the persons with normal plasma proteins we found a mean IIp of 26.9 mmHg, a mean IIi of 15.8 mmHg on the thorax, and a mean IIi of 11.1 mmHg on the lower leg. A fall of IIp from normal values to 16.5 mmHg caused a fall in IIi of about 8 mmHg on the thorax and about 7 mmHg on the leg without oedema formation. In patients with IIp from 16.0 mmHg down to 8.0 mmHg, IIi did not change very much, and was about 5.5 mmHg on the thorax and 2.6 mmHg on the leg. These results support the view that reduction of IIi plays an important role as an oedema preventing factor in patients with hypoproteinaemia.

Interstitial fluid colloid osmotic and hydrostatic pressures in subcutaneous tissue of patients with nephrotic syndrome

Interstitial fluid colloid osmotic and hydrostatic pressures in subcutaneous tissue of patients with nephrotic syndrome

Interstitial protein ‘wash‐down’, an early sign of cardiac failure?

Summary. An increase of interstitial fluid volume (IFV) with or without clinical oedema is an important sign of congestive heart failure. Without entering into a discussion of forward versus backward failure, we will briefly analyse this alteration of trans‐capillary fluid balance in peripheral tissues: the rise in IFV must result either from a rise in net capillary filtration, or from a decrease of lymph flow. Since lymph flow is increased rather than decreased in congestive heart failure (Langgård, 1963), we must conclude that a rise in IFV is caused by increased net capillary filtration. According to the Starling equilibrium, a rise in net filtration could result from (a) a rise in average capillary pressure (Pc), (b) a reduction of interstitial fluid hydrostatic pressure (Pi), (c) a fall in plasma colloid osmotic pressure (COPP), or from (d) an increase of interstitial fluid colloid osmotic pressure (COPi), Since COPp and Pi are normal in most cases of congestive heart failure, and since COP; and Pi tend to change opposite to the required direction (see below), it follows that the rise in IFV results mainly from a rise in mean capillary pressure.

Compliance of the interstitial space in rats. II. Studies on skin.

Interstitial compliance, defined as the ratio between changes in interstitial fluid volume (delta IFV) and interstitial fluid pressure (delta IFP), has been measured for rat skin. IFP has been measured with sharpened glass capillaries connected to a servocontrolled counterpressure system, while IFV has been determined as the extravascular distribution space for 51Cr-EDTA. The measurements were performed at hydration and dehydration of various duration. Compliance was 0.162 ml/g dry tissue per mmHg in dehydration, corresponding to 5.4 ml/100 g wet tissue per mmHg. The volume-pressure curve was similar at 2-4 and 24-28h of dehydration. Up to 20% increase in IFV compliance was similar to that in dehydration, but thereafter increased severalfold upon further increase in IFV. Even at sixfold increase in IFV, IFP did not rise by more than 1 to 2 mmHg. Control IFV in skin amounts to 40 ml/100 g wet tissue and IFV will therefore change by 14% when IFP changes by 1 mmHg from the control level. This change in IFV will cause interstitial fluid colloid osmotic pressure to increase or decrease by somewhat more than 1 mmHg in dehydration or hydration respectively from a normal control level of about 9 mmHg. With further increase in IFV secondary to increased capillary filtration, the interstitial edmaprevention will depend on washout and/or dilution of interstitial proteins since IFP did not increase by more than 1 to 2 mmHg.

Compliance of the interstitial space in rats. I. Studies on hindlimb skeletal muscle.

Interstitial compliance, defined as the ratio between changes in interstitial fluid volume (delta IFV) and interstitial fluid pressure (delta IFP), was determined for rat skeletal muscle. IFV was measured as the extravascular distribution space for 51Cr-EDTA, while sharpened micropipettes connected to a servo-controlled counterpressure system were used to measure IFP. The experimental protocol was designed to bring about acute (2-4 h) and chronic (24-28h) tissue over- and dehydration. During dehydration, the average compliance was 0.056 ml/g dry weight . mmHg, corresponding to 1.40 ml/100 g wet tissue . mmHg, and was not significantly different in acute and chronic experiments. In hydration (acute and chronic), compliance increased several-fold when IFV increased. Even at greatly increased IFV, IFP did not rise more than 1 to 1.5 mmHg above control level. Since control IFV amounts to 10 ml/100 g wet tissue, IFV will decrease by 14% when IFP falls by 1 mmHg from this control level. Provided unchanged interstitial protein mass the dehydration will cause interstitial fluid colloid osmotic pressure to increase by somewhat more than 1 mmHg--from a control level of 9 mmHg. Furthermore, since IFP was not increased by more than 1 to 1.5 mmHg during hydration, an increase in IFP plays a minor role in edema-prevention compared to dilution and/or washout of interstitial proteins.

Interstitial fluid volume, colloid osmotic and hydrostatic pressures in rat skeletal muscle. Effect of hypoproteinemia.

Colloid osmotic pressures in plasma (COPp) and interstitial fluid (COPi), interstitial fluid pressure (Pi) as well as interstitial fluid volume (IFV) was measured in rat skeletal muscle during development of hypoproteinemia. The hypoproteinemia was induced with intraperitoneal injections of aminonucleoside puromucin causing a renal lesion similar to that in human nephrotic syndrome with renal loss of plasma protein and subsequent fall in COPp. When COPp fell from control values (about 20 mmHg) to about 10 mmHg, the fall was accompanied by an identical fall in COPi (in mmHg) while Pi did not change. Provided the pre- to postcapillary resistance ratio was unchanged, the pressure imbalance in the Starling forces (net filtration pressure) was similar to the control situation at this stage of the hypoproteinemia. With further fall in COPi, the absolute fall in COPi was less, - leading to increased net filtration pressure, and finally edema appeared. In presence of edema, Pi rose from average control values of -0.20 mmHg to an average of +1.5 mmHg. Interstitial fluid volume in hypoproteinemic rats without edema was similar to that of controls (about 0.30 ml/g dry tissue), and increases to 3 to 4 times this value in the presence of edema. Comparing the fall in COPi to IFV in the nephrotic rats without edema show that the fall in COPi must have been brought about by a lymphatic washout of interstitial proteins since IFV was similar to the controls when COPi had fallen to 1/3 that of control.

Albumin concentration and colloid osmotic pressure of interstitial fluid collected by wick technique from rat skeletal muscle. Evaluation of the method.

Interstitial fluid from rat skeletal muscle has been collected by multifilamentous nylon wicks. The wicks consisted of 5-600 single filaments and had an overall diameter of 1-2 mm. The wicks were implanted in the muscle by means of a mending needle. The wicks were removed at various times after implantation, and colloid osmotic pressure (COP) or albumin concentration in wick fluid was measured. The fluid contained in the wick had a COP of 8-10 mmHg and an albumin concentration about 1/3 that of plasma. COP in wicks preloaded with serum of serum/saline dilution was higher after 1/2 and 1 h of implantation, but was nearly identical to that of saline soaked wicks after 2 h implantation. Intravenous injection of labelled albumin showed that wick implantation caused a marked leakage of proteins from plasma to the wick. However, 1/2 to 1 h after implantation the leakage was markedly reduced. The initial leakage of albumin could be diminished with protease inhibitor (aprotinin), but not with prostaglandin-, serotonin-, or histamine antagonists. The experiments show that wick fluid colloid osmotic pressure reflects interstitial fluid colloid osmotic pressure, while the protein composition of wick fluid may not be identical to that of undisturbed interstitial fluid.

Intraperitoneal pressure: ascitic fluid and splanchnic vascular pressures, and their role in prevention and formation of ascites.

Seventeen patients with ascites due to cirrhosis underwent hepatic venous catheterization and pressure measurement in the ascitic fluid. Intraperitoneal fluid hydrostatic pressure (IFP) ranged 3.5-22, mean 11.2 mm Hg, and correlated closely to the pressure in the inferior vena cava (r = 0.97, P < 0.001), which was on average 1.8 mmHg above that of ascitic fluid (P < 0.005). Wedged hepatic venous pressure (WHVP) (range 19-43, mean 32 mmHg) correlated directly to IFP (0.89, P < 0.001) and was significantly higher than that of ten cirrhotic patients without ascites (range 12-27, mean 20 mmHg, P < 0.005). After diuretic therapy WHVP decreased to an average of 20 mmHg. Mean plasma colloid osmotic pressures were 20 mmHg (range 18-24 mmHg)( and 23 mmHg (range 19-29 mmHg) in patients with and without ascites, the values being significantly different (P < 0.05). Colloid osmotic pressure of ascitic fluid ranged 1-14, mean 4.9 mmHg. Mean ratio between albumin concentration in ascitic fluid and plasma was 0.31 (range 0.12-0.77). In five pigs portal venous pressure (PVP) increased during infusion of fluid into the peritoneal cavity. The increase in PVP was smaller than that of IFP (P < 0.02), indicating that ascitic fluid stems the pressures in the splanchnic venous vascular bed up to a higher level, but that the transmural hydrostatic pressure difference decreases simultaneously. The results are discussed in relation to the local 'oedema-preventing' mechanisms: (a) increased interstitial hydrostatic fluid pressure, (b) decreased interstitial fluid colloid osmotic pressure, (c) increased lymph flow, and it is concluded that the peritoneal space can be considered as a special part of the interstitium in which IFP is considered to play an important role in regulation of ascitic fluid.

Pathogenesis of oedema in protein-energy malnutrition: the significance of plasma colloid osmotic pressure.

1. Rats were made oedematous by feeding them low-protein diets (protein: energy (P:E) 0.005) ad lib., and measurements were made of plasma and interstitial fluid colloid osmotic pressures (πp and πi respectively) and interstitial fluid hydrostatic pressure (Pi) before, and at the onset of, oedema formation. Taken together as (πp − πi + Pi) these forces oppose capillary pressure (Pc) and thus determine rates of transcapillary water filtration. Interstitial fluid was sampled, in non-oedematous and oedematous animals, from perforated capsules implanted subcutaneously for the measurement of Pi. Blood, plasma and interstitial fluid volumes were also determined.2. In Expt I comparisons were made between animals fed on a control diet (P:E 0.210) and the lowprotein diet. In normal animals the ratio πp:πi was approximately 2, but in protein deficiency it was increased since reductions in the absolute value of πi matched those in πp. These changes were observed 2 weeks after the start of the experiment and became more exaggerated when oedema appeared (weeks 18–22).3. Pi was normally negative with respect to atmospheric pressure but increased to values close to zero when oedema formation occurred.4. Despite the reductions in πp that were seen in the protein-deficient animals the sum of the forces opposing filtration (πp − πi + Pi) did not change significantly during the experiment.5. Plasma and interstitial fluid volumes expressed per kg body-weight (measured using 125I-albumin and 35SO42−) were unchanged as πp initially decreased in the protein-deficient animals but increased markedly with the onset of oedema.6. In Expt 2 comparisons were made between animals fed the low-protein diet ad lib. and others fed on the control diet in restricted amounts so that weight loss was the same in the two groups of animals.7. The wasting induced by restriction of the control diet did not produce reductions in πp or πi and values for Pi were normal. Changes in the animals fed on the low-protein diet were similar to those observed in Expt I. By using 51Cr-labelled erythrocytes it was shown that the expansion in plasma volume that occurred when oedema appeared in the protein-deficient animals was mainly due to a reduction in total erythrocyte volume. Blood volume did not increase significantly.8. It was concluded that in the hypoproteinaemia induced in the experimental animals reductions in the value of πp, which might otherwise result in an imbalance of forces that would produce excessive rates of transcapillary water filtration, were compensated for by reductions in πi. Increases in Pi also compensated but were quantitatively less important.9. The significance of the results is discussed in terms of the pathogenesis of oedema in kwashiorkor and the concept of an oncotic threshold for oedema formation in hypoproteinaemia.

An implantable colloid osmometer: Measurements in subcutis and skeletal muscle of rats

An implantable colloid osmometer has been developed for measurement of interstitial fluid colloid osmotic pressure (CO P i). Amicon hollow fibres with a cutoff at MW 10,000 were used as a semipermeable membrane. The osmometer has a length of 10–15 mm, an outer diameter of 0.35 mm, and is connected to a pressure transducer via a PE 20 catheter. The equlibration time was about 10 min. In vitro comparison to an ordinary membrane osmometer showed a coefficient of correlation of 0.99. When the osmometer is implanted in tissue, the pressure transducer read the sum of -CO P i (CO P measured as a negative hydrostatic pressure, but defined as positive) and interstitial fluid hydrostatic pressure ( P i, positive or negative). In other words, the sum of the “interstitial Starling pressures” is measured directly. After perforation of the membrane, only P i will be recorded. With intact membrane, implantation in rat subcutis (18 measurements in 8 rats) gave an average pressure of −10.8 (SD, 1.4) mm Hg. In skeletal muscle (17 measurements in 7 rats), the average pressure was −8.6 (SD, 2.1) mm Hg. With perforated membrane, pressures between −1 and 0 were obtained in both tissues, giving a CO P i of about 10 mm Hg in subcutis and 8 mm Hg in muscle. An increased pressure (less negative) could be recorded continuously or by reimplantation, while furosemide diuresis reduced the pressure.