Changes In Colloid Osmotic Pressure Research Articles

Regulation of albumin and α-fetoprotein gene expression by colloid osmotic pressure in human hepatoma cells

Background: Colloid osmotic pressure has been thought to regulate albumin synthesis; however, the exact mechanism remains obscure. In the present study, the effect of colloid osmotic pressure on the albumin and α-fetoprotein gene expression in HuH-7 human hepatoma cells was analyzed. Methods: HuH-7 cells were treated with albumin or dextran (mean mol wt, 70,000), and changes in the levels of albumin and α-fetoprotein messenger RNA (mRNA) were analyzed by Northern blotting. Furthermore, in transient chloramphenicol acetyltransferase (CAT) plasmid transfection experiments, effects of colloid osmotic pressure on CAT activities were studied. Results: By Northern blot analysis, the levels of both albumin and α-fetoprotein mRNA were dose-dependently suppressed by the elevation of colloid osmotic pressure and returned to pretreatment levels 48 hours after the culture medium containing dextran was replaced with a dextran-free fresh medium. In transient CAT plasmid transfection experiments, the increased level of colloid osmotic pressure resulted in the repression of both albumin and α-fetoprotein promoter activities. In contrast, α-fetoprotein enhancer activity, which possibly regulates not only α-fetoprotein but also albumin gene expression, was not affected by changes in colloid osmotic pressure. Conclusions: These results suggest that colloid osmotic pressure regulates both albumin and α-fetoprotein gene transcription through the modulation of their promoter activities.

Albumin, HES 120 and dextran 70 as adjuvants to red blood cell concentrates: a study on colloid osmotic pressure changes in vitro

An in vitro model of surgical bleeding was developed to simulate continuous blood loss and replacement therapy with plasma substitutes and red cell concentrates. The model was used to determine the lowest colloid concentration in vitro for each of the plasma substitutes that sustains colloid osmotic pressure above 2.4 kPa (or 18 mmHg) when used up to the recommended maximal total dose. Plasma, supernatant separated from red cell concentrates and dextran 70, hydroxyethyl starch 120 or albumin were mixed to create dilutions imitating plasma composition in the course of clinical blood loss and replacement therapy. The relative volume of each component was calculated according to the model when the bleeding was equal to multiples of 10% of blood volume up to a blood loss of 120%. Our measurements indicate that the colloid concentrations of 5.0% for albumin, 4.0% for hydroxyethyl starch 120 and 3.5% for dextran 70 preserve colloid osmotic pressure above 2.4 kPa.

Forces involved in transcapillary fluid movement in exercising cat skeletal muscle

Average capillary pressure (Pc) close to the venous end (fluid equilibrium point) of the exchange vessels (denoted Pc,v), arterial (PA) and venous pressure, and the rate of net transcapillary fluid flux were continuously recorded in sympathectomized muscle during 30 min of graded exercise and for 30 min in the post-exercise period. Regional changes in colloid osmotic pressure (pi pl) and total osmolality in plasma, the latter reflecting work-induced interstitial hyperosmolality, were measured at intervals. In the control state at rest with a Starling fluid equilibrium, Pc,v averaged 17.6 +/- 0.8 mmHg. Exercise caused a rapid transcapillary plasma fluid loss, the net driving pressure for which in the initial phase of heavy work was 58 mmHg (transcapillary fluid flux divided by the capillary filtration coefficient). This comprised an increase in Pc,v of 16 mmHg, a nonprotein osmotic force (Posm) related to exercise-induced tissue hyperosmolality corresponding to 46 mmHg and an opposing force established by a raised pi pl of 4 mmHg. A theoretical analysis indicated that the main fraction of the osmotic fluid loss passed through transcellular ultrapores and only a minor part through conventional small pores. In spite of the fact that Pc remained high throughout the exercise period, the outward fluid flux gradually declined and a Starling equilibrium was re-established 23 min after the commencement of heavy exercise. This was explained by a gradual decline of Posm and apparently also by a secondary increase in tissue pressure (Pif) and/or a decrease in interstitial colloid osmotic pressure (pi if). Net fluid absorption occurred in the post-exercise period as a result of a gradual decrease in Pc, reversed transcapillary Posm and also maintained high Pif and/or low pi if. Exercise (even light) abolished normal Pc autoregulation, implying that the filtration component of net transcapillary fluid flux becomes distinctly modulated if PA is altered.

Considerations for Anesthetic Management During Veno-venous Bypass in Adult Hepatic Transplantation

Intraoperative data from 42 adult orthotopic hepatic transplant recipients were analyzed retrospectively to assess the hemodynamic, coagulation, and thermal effects of heparinless veno-venous bypass using a constrained vortex pump. Transient hemodynamic changes occurring at the onset of bypass included decreases in temperature (-10.7%), heart rate (-18.7%) and arterial pressure (-15.1%); and increases in central venous pressure (27.6%) and ECG T wave amplitude (231.6%). Abrupt decreases in cardiac output and pump flow occurred with termination of the portal limb of bypass, which is required to allow completion of the portal vein anastomosis. However, significant continuous decreases were observed in bypass flow and cardiac output during the entire bypass period. The blood volume became concentrated as indicated by increases in hematocrit, colloid osmotic pressure, serum osmolality and serum sodium. Changes in colloid osmotic pressure were inversely related to bypass flow. These data, along with an accumulating base deficit, suggest that veno-venous bypass is associated with less than optimal perfusion of the abdomen and lower extremities. Flow dependent third space fluid accumulation is most likely responsible for decreasing cardiac output and pump flow during the bypass period. No clinically significant coagulopathy could be attributed to the use of veno-venous bypass. There were no significant changes in platelet counts, fibrinogen levels or prothrombin times. The activated partial thromboplastin time decreased from 60.5 to 50.2 seconds. Patient core temperature decreased three times more rapidly (0.9 degrees C/hr) during bypass than at any other time during the procedure.

Colloid Osmotic Pressure in Pulmonary Edema Clearance with Furosemide

After tripling of baseline lung water (EVLW), decreasing wedge pressure (PWP) alone for two hours did not decrease EVLW. In 11 of 16 dogs, triple baseline EVLW and a decrease in plasma colloid osmotic pressure (COP) from 21.1 +/- 0.8 to 17.8 +/- 0.8 mm Hg resulted from left atrial balloon inflation at PWP of 28 to 30 mm Hg. With subsequent lowering of PWP to 10 mm Hg, intravenously administered furosemide (1 mg/kg) was given to these 11 dogs. One half hour after furosemide, shunt decreased slightly without decreasing EVLW in all 11 dogs, but by two hours, seven dogs (group 1) decreased EVLW (from 23.2 +/- 1.8 to 11.1 +/- 1.4 ml/kg) and shunt (37.4 +/- 2.0 to 12.9 +/- 2.9 percent), while four dogs (group 2) did not (EVLW: 22.3 +/- 1.4 to 22.5 +/- 0.6 ml/kg: shunt, 36.8 +/- 1.7 to 36.5 +/- 1.9 percent). Group 1 had diuresis, maintained normal blood urea nitrogen and creatinine levels, and increased COP from 17.7 +/- 0.7 to 23.6 +/- 0.5 mm Hg while group 2 was oliguric with elevated BUN and creatinine values and showed no change in COP (17.9 +/- 0.9 to 18.3 +/- 0.6 mm Hg) after furosemide. After decreasing PWP in massive pulmonary edema (triple baseline EVLW), furosemide appeared to enhance edema clearance by changes in COP with diuresis.

Cardiovascular Effects of Vena-Venous Bypass during Hepatic Transplantation

(J. Extra-Corpor. Technol. 19[3] p. 268-273 Fall 1987, 12 ref). A series of 42 orthotopic hepatic transplant patients were reviewed retrospectively to determine the cardiovascular effects of heparinless venavenous bypass using a constrained vortex pump. Pump flows and cardiac outputs fell progressively during bypass. During the bypass period the vascular volume became hemoconcentrated as indicated by increases in hematocrit, colloid osmotic pressure, serum osmolality, and serium sodium. The changes in colloid osmotic pressure were inversely related to the bypass pump flow. Transient hemodynamics occurring at the onset of bypass included decreases in temperature, heart rate, arterial pressure, and increases in pulmonary artery pressure, central venous pressure and T wave amplitude. Core temperature changed at the rate of -0.89°C per hour during the bypass period as compared to -0.31°C during the previous phase of the procedure. Veno-venous bypass may improve hemodynamic stability during the anhepatic phase of the procedure, but the abdomen and lower extremities may be less than optimally perfused.

Decreasing Hydrostatic Pressure Does Not Uniformly Decrease High-Pressure Pulmonary Edema

Pulmonary artery wedge pressure (PAWP) of 30 mm Hg with left atrial balloon inflation for 1 1/2 hours produced pulmonary edema in eight dogs. PAWP was then decreased to 10 mm Hg for two hours, and shunt, lung water (extravascular thermal volume, or ETV, by thermal dye), and perfusion distribution (radiomicrosphere technique) were measured and compared with four other dogs (group 1) whose PAWP was maintained at 10 mm Hg. The eight dogs with PAWP of 30 mm Hg for 1 1/2 hours were retrospectively subdivided into two groups of four based on ETV (group 2, double baseline ETV; group 3, triple baseline ETV). Baseline ETV and shunt were similar for all groups and remained unchanged for group 1. At 1 1/2 hours, 2 hours (1/2 hour after decreasing PAWP), 2 1/2 hours, and 3 1/2 hours, respectively, ETV were: 13.9 +/- 1.9, 12.8 +/- 2.0, 9.3 +/- 1.5, and 8.5 +/- 1.0 ml/kg in group 2; and 21.9 +/- 2.1, 22.7 +/- 2.2, 22.5 +/- 2.0, and 22.2 +/- 2.0 ml/kg in group 3. A more variable rate of edema formation was detected in eight additional dogs, but failure to resolve higher levels of edema after decreasing PAWP was also demonstrated in this group. Edema was greatest in lower lobes and decreased lobar perfusion. Shunt was higher in group 3 than in group 2 at 1 1/2 hours and decreased in group 2 but not in group 3 at 3 1/2 hours. Changes in colloid osmotic pressure may account for the differences in edema formation and resolution, but our data suggest that, independent of the rate of edema formation, a decrease in vascular exchange surface area at higher levels of edema may inhibit edema resolution when PAWP is decreased.

Colloid osmotic pressure changes in human whole blood and separated plasma in vitro with changes in CO 2 content and pH

1. 1. Colloid osmotic pressure (COP) and pH were measured on the true plasma of human blood from five subjects tonometered with different concentrations of carbon dioxide. Measurements were also made on their separated plasma. 2. 2. COP (mmHg) of true plasma obtained from tonometered whole blood varied in proportion to the bicarbonate concentration (mEq/1): COP = 0.056 [HCO 3 −] + 23.3 3. 3. In separated plasma, as CO 2 concentration increased, COP decreased as pH decreased: COP = 1.99 (pH) + 11.0. 4. 4. When the change in COP due to the change in pH was subtracted from the observed change of COP due to CO 2 exposure of whole blood, the difference was the change of COP due to the shift of fluid between plasma and red cells: COP adjusted for pH = 0.131 [HCO 3 −] + 21.5. The COP values of tonometered whole blood and separated plasma are taken to be equal at a pH of 7.40 (at the mixed venous point). 5. 5. The change in COP, adjusted for pH, for a given change in pCO 2 is in keeping with the amount of fluid shift calculated from the measured changes in hematocrit and plasma protein concentration. 6. 6. An error in a previous paper (Kakiuchi et al., J. appl. Physiol. 44, 474–478, 1978) had led to an overestimation of the COP change from the exposure of whole blood to CO 2 in vitro.

Circulatory arrest pressure as a prognostic indicator of cardiopulmonary resuscitation.

In a porcine model of cardiac arrest, the intravascular pressure measured during circulatory standstill was positively correlated with the success of cardiopulmonary resuscitation. When volume was expanded before cardiac arrest, circulatory arrest pressure increased and the success of resuscitation increased. After volume expansion, the hematocrit was reduced and colloid osmotic pressure was decreased. However, neither hematocrit nor colloid osmotic pressure changes were directly related to survival.

Peripartum colloid osmotic pressure changes: Effects of controlled fluid management

A prospective, fluid-controlled study of serially measured colloid osmotic pressure changes in the peripartum period was undertaken. Seventeen patients with uncomplicated pregnancies undergoing elective cesarean section at term were administered a predelivery bolus of 15 ml/kg of lactated Ringer's solution prior to operation. Maintenance crystalloid fluids were infused at 125 to 150 ml/hr both intraoperatively and post partum without the addition of blood or other colloid solutions. Serial colloid osmotic pressure measurements were obtained before hydration, after hydration, after delivery, and at 6 and 24 hours post partum. The results demonstrated a 15.9% decline in colloid osmotic pressure immediately following the hydration bolus (20.7 ± 1.5 to 17.4 ± 1.8 mm Hg) (p < 0.01). A further decline in colloid osmotic pressure to 16.6 ± 1.7 mm Hg occurred after delivery and represented an overall 22% decrease from the baseline value (p < 0.05). The lowest mean colloid osmotic pressure value occurred at 6 hours post partum (16.1 ± 1.1 mm Hg). These data support previous observations that colloid osmotic pressure is uniformly lowered in the immediate postpartum period with peak reductions identified at 6 hours following delivery. In addition, intravenous crystalloid administration during the peripartum interval can substantially influence this decline in colloid osmotic pressure. Although no clinical evidence of cardiopulmonary compromise was observed in this set of normal gravid women, these data may be useful in the management of the parturient patient with established risk factors for pulmonary edema where alterations in the pulmonary capillary wedge pressure-colloid osmotic pressure gradient have been shown to correlate with the development of this complication.

Colloid osmotic pressure changes in isolated isogravimetric cat hindlimb.

The development of osmotic pressure, following the addition of bovine serum albumin (BSA) to the perfusate, was measured in an isogravimetric cat hindlimb fully dilated with papaverine. The changes in colloid osmotic pressure were followed by recording the changes in venous pressure (PVI) necessary to maintain constant weight. Capillary filtration coefficient (CFC) and vascular compliances were calculated from weight changes following steps in venous pressure. Venous BSA levels reached arterial within 1 min, and PVI reached a new steady state 13.1 +/- 0.9 (SE) min (n = 9 in 6 limbs) after adding BSA. This apparent delay in the development of the osmotic pressure agrees with earlier reports. However, when the BSA was added under constant venous pressure conditions, the fluid reabsorption reached its maximum rate within 1.5 min. The data suggest that the BSA is osmotically fully effective after the capillary washin. The slowness of the rise of PVI in the isogravimetric state is probably caused by the time necessary to absorb sufficient fluid from the interstitium to raise the capillary pressure to a level that balances the increased oncotic pressure. A mathematical model supports this explanation.

Colloid osmotic pressure changes during hypertensive pregnancy.

Colloid osmotic pressure (COP) was measured in maternal serum of normal and hypertensive gravidae, and in their amniotic fluid. Both normal and hypertensive gravidae in the third trimester at bed rest and those treated for hypertension have low COP. Likewise, postpartum women may have low serum COP values apparently unrelated to any disease process. Amniotic fluid COP is low in both normal and hypertensive gravidae. COP Measurements therefore, seemingly offers little information regarding the health of pregnant women. Serum COP may increase in some hypertensive gravidae receiving saline infusion, probably reflecting abnormal renal function and hypovolemia. High serum triglyceride values coexisting with low COP may represent hepatic efforts to produce other colloid osmotic-active substances in the semi-chronic situation, although our findings in the acute situation did not support this hypothesis.

Changes in colloid osmotic pressure in patients undergoing cardiothoracic surgery

Measurements of plasma colloid osmotic pressure (COP) were made during and for 24 h after normothermic continuous flow cardiopulmonary bypass (CPB) in 20 adults exposed to sudden haemodilution by a crystalloid pump prime solution. Haematocrit, albumin and total protein were also measured. Within 5 min of starting bypass the mean COP fell to 45% pre-bypass value and remained at this level until bypass was discontinued. Following bypass, the oncotic pressure rose rapidly during the first hour to 84% of the prebypass value, and then more slowly until it reached the pre-bypass value 24 h later. The trend seen for plasma proteins and haematocrit was similar but the fall was smaller, 65-70% of the pre-bypass values. This significant difference in fall between plasma protein concentration and directly measured COP is explained by their non-linear relationship. Three patients died soon after bypass. They all showed significantly lower values of COP than the mean for the group as a whole at some stage (P less than 0.05).

Critical care problems in neonates. Colloid osmotic pressure in healthy and sick neonates.

Clinical usefulness of colloid osmotic pressure (COP) measurements in adults has been well established. However, data in healthy and sick neonates are sparse. The present study established the COP changes in healthy term and preterm infants and in critically ill neonates. COP in healthy term (16.9 +/- 1.9 mm Hg) and preterm (15.4 +/- 1.3) infants was significantly lower than adults (21.6 +/- 3.6). Even in sick neonates, COP correlated with gestational age (n = 78, r = 0.63, p less than 0.001 , birth weight (r = 0.58, p less than 0.001) and total protein (n = 71, r = 0.58, p less than 0.001). Critically ill preterm infants with hyaline membrane disease had the lowest COP (11.5 +/- 1.2). Administration of 10% albumin failed to increase the COP significantly. In critically ill preterm infants who survived, the COP increased during the first postnatal week, whereas in nonsurvivors COP decreased significantly to less than 10 mm Hg.

Phthalaldehyde microprotein method: Usefulness and potential errors

Two major technical advances introduced by Brenner et al [l, 2] have been responsible for recent breakthroughs in understanding the process of glomerular ultrafiltration at the single nephron level. These are the development of a method for directly measuring glomerular capillary pressure [1] and the microadaptation of the colorimetric protein method of Lowry et al [2, 3] to estimate changes in colloid osmotic pressure between the afferent and efferent ends of the glomerular vasculature [4]. The good correlation between colloid osmotic pressure as calculated from the arterial protein concentrations and direct measurement of the colloid osmotic pressure has established the usefulness of the protein method to accurately measure intravascular oncotic forces [5]. Because the colorimetric Lowry microprotein method is both time consuming and necessitates the use of a frequently unstable, relatively high intensity colorimetric scale for sample reading, attempts have been made to use other microprotein techniques as substitutes for the Lowry method [6–9]. Viets et al [7] have compared the usefulness of two fluorescent microprotein methods in micropuncture studies. Of these, the phthalaldehyde fluorescent microprotein method was preferable and appeared to be equally as useful as the Lowry method, with certain minor limitations. Our laboratory has spent the last 2 years evaluating the applicability of the phthalaldehyde technique to microprotein analysis in micropuncture studies. Although we have found the method to have the advantage of being less time consuming than the Lowry technique, we have noted certain limitations and potential errors that could artificially lower the estimate of protein content in plasma samples. Spuriously low protein concentrations could result in under-estimations of afferent and efferent arteriolar oncotic pressures and overestimates of single nephron filtration fractions. This report is designed to describe the limitations of phthalaldehyde fluorescent protein technique and point out its potential errors in measuring protein concentration while comparing its usefulness to that of the colorimetric micro-Lowry method.

Colloid osmotic pressure changes of dog's blood exposed to different mixtures of CO2 and air.

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.

Interaction of capillary and tissue forces in the cat small intestine.

We measured steady state capillary hydrostatic pressure (P c,i), plasma and lymph protein concentrations, lymph and blood flow, and capillary filtration coefficients in an in situ loop of cat small intestine at venous outflow pressures (PV) of 0, 5, 10, 15, 20, 25, and 30 mm Hg. The data were used to calculate colloid osmotic pressure of lymph and plasma, interstitial fluid pressure (Pt), pre- and postcapillary resistances, and a tissue pressure-volume curve of the intestinal interstitium. When PV was elevated from 0 to 30 mm Hg, lymph protein concentration decreased from 3.8 to 1.9 g/100 ml (representing a change in colloid osmotic pressure of 6.2 mm Hg), lymph flow increased 7-fold (or an equivalent imbalance in Starling forces of 4.3 mm Hg), and the calculated PT increased from 1.8 to +5.3. Because lymph flow draining the loop decreased during the determination of Pc, i at venous pressures between 15 and 30 mm Hg, the corresponding calculated PT may be in error by 1-2 mm Hg. The tissue pressure-volume relationship calculated from the data indicates that the intestinal interstitial volume expands nonlinearly and this expansion is characterized by two distinctly different compliant components: (1) tissue compliance is low at PV between 0 and 15 mm Hg (0.4 ml/mm Hg), and (2) at PV greater than 15 mm Hg the tissue compliance is relatively high (4 ml/mm Hg). We found that when PV was elevated from 0 to 15 mm Hg, increases in PT are the major tissue adjustments that oppose the increased filtration pressures. Furthermore, at Pv of 20-30 mm Hg, tissue protein concentration decreases, lymph flow relative to the filtration coefficient (deltaP DROP) increases and, to a much lesser extent, PT increases. Finally, the combination of these changes in tissue force at high filtration pressures represent a maximum tissue edema "safety factor" of 10 mm Hg; further increases in filtration pressures result in large volume movements into the intestinal lumen.

Transport of molecules across renal glomerular capillaries.

Direct measurements of the pressures and flows governing the formation of glomerular ultrafiltrate have been made possible in recent years by virtue of 1) the discovery of rats and monkeys possessing glomerular capillaries on the renal cortical surface, accessible to micropuncture, and 2) technological advances that permit measurement of intracapillary hydraulic pressure and assessment of the change in colloid osmotic pressure along the glomerular capillary network. Based on these direct measurements, evidence has been obtained to indicate that glomerular capillary hydraulic pressure and hence the net driving force for ultrafiltration are lower than previously believed. By the efferent end of the glomerular capillary network, net filtration of fluid ceases, owing to a reduction in the net driving force to zero. Evidence in the rat indicates that the process of ultrafiltration is highly dependent on glomerular plasma flow rate. Studies in rats with surface glomeruli have also made possible an assessment of the factors that govern the transport of macromolecules across the highly specialized capillary network. In addition to molecular size, transcapillary movement of macromolecules is influenced by the glomerular filtration rate, since total transport reflects the combined contributions of convection as well as diffusion. Molecular charge has also been found to be an important determinant of the transport of macromolecules, very likely contributing to the marked restriction to the transcapillary movement of albumin. This electrostatic restriction to the transport of polyanions such as albumin, by some fixed, negatively charged component(s) of the glomerular capillary wall, is markedly reduced in primary glomerular injury. Evidence indicates that glomerular injury results in loss of these fixed negative charges from the capillary walls, providing an attractive explanation for the enhanced filtration of albumin, and hence the proteinuria, observed in a variety of glomerulopathic states.

Colloid osmotic pressure fluctuations and the disequilibrium syndrome during hemodialysis.

Changes in colloid osmotic pressure (COP), osmolality, blood urea nitrogen, glucose, electrolytes and arterial blood gases were correlated with the symptoms that occurred during 46 dialyses in 10 stab

Changes in colloid osmotic pressure during and shortly after open intracardiac operation

Changes in colloid osmotic pressure during and shortly after open intracardiac operation