Plasma Colloid Oncotic Pressure Research Articles

The Effect of Oral Albumin Intake on Serum Albumin Levels in Preeclamsia Patients With Hypoalbuminemia in RSUP Dr. M. Djamil Padang

Introduction : Albumin main function is maintaining the plasma colloid oncotic pressure. Preeclampsia cause a decrease in serum albumin in the pregnant woman. Low albumin levels increase mortality, longer wound healing and longer hospital stays. The intake of oral albumin is expected to be effective in increasing the level of albumin in the blood.Objective : To determine the effect of freeze dryer method intake compared to liquid snakehead fish extract in patients with preeclampsia and hypoalbuminemia.Material and methods : Using pre and post-test control group design.The total sample was 38 patients with severe preeclampsia with hypoalbuminemia, divided into control and intervention groups. Control was given the intake of liquid snakehead fish extract, in the intervention was given the Freeze dryer method. The research data were analyzed using the Mann Whitney test method and the Wilcoxon test.Results : In the intervention group the mean pretest albumin level was 2.66 ± 0.17 gr / dl and on the 4th day it was 3.13 ± 0.16 gr / dl (p = 0.000). In the control group the mean pretest albumin level was 2.72 ± 0.15 gr / dl and on the 4th day it became 3.06 ± 0.14 gr / dl (p = 0.000). On the 4th day after treatment, the increase in serum albumin levels in the intervention group was 0.47 ± 0.19 gr / dl; whereas in the control group was 0.34 ± 0.10 gr / dl with a value of p = 0.031 (p <0.05).Conclusion : The freeze dryer method (freeze dryer method ) for the Cork Fish Extract resulted in a higher increase in albumin levels than the liquid snakehead fish extract.Keywords: Preeclampsia, Hypoalbuminemia, freeze dryer method of Snakehead Fish Extract

Low albumin levels are associated with mortality in the critically ill: A retrospective observational study in a multidisciplinary intensive care unit.

Background Albumin is a determinant of plasma colloid oncotic pressure and buffering capacity. It is a carrier protein for drugs and is important for normal functioning of the glycocalyx. Hypoalbuminaemia is common in the critically ill and has been associated with adverse outcomes. The association between hypoalbuminaemia and outcome has not been specifically explored in the South African context. Objectives To determine whether albumin levels on admission and changes in albumin levels were associated with intensive care unit (ICU) mortality in a heterogenous critically ill population. Methods This was a retrospective observational study of 247 adult patients who were admitted to a multidisciplinary ICU. Albumin levels were measured on admission and 48 hours later, alongside other biochemical and clinical parameters to determine whether they were predictive of ICU mortality. Results The lowest level of albumin on admission was 8 g/L and the highest was 43 g/L. The incidence of hypoalbuminaemia (using the laboratory reference range) was 93.9% on admission and 99.4% at 48 hours. Receiver operating characteristic curve analysis provided an optimal albumin cut-off of 18.5 g/L. Using this cut-off, hypoalbuminaemia at admission and at 48 hours was associated with increased ICU mortality. Hypoalbuminaemia at admission was an independent predictor of mortality using multivariable analysis (OR 3.74; 95% confidence interval 1.87 - 4.48). Conclusion Hypoalbuminaemia is associated with increased ICU mortality. There is currently no evidence to support the use of albumin replacement therapy. Further research is required to determine its role in critically ill patients. Contributions of the study Hypoalbuminaemia is common in critically ill South African (SA) patients and is associated with increased ICU mortality. This has not been well explored in the SA setting. We found that an optimal albumin cut-off was 18.5 g/L, which was much lower than the limits of the laboratory reference range.

Effect of Coagulation Factor Concentrates on Markers of Endothelial Cell Damage in Experimental Hemorrhagic Shock.

Plasma-based resuscitation showed protective effects on the endothelial glycocalyx compared with crystalloid resuscitation. There is paucity of data regarding the effect of coagulation factor concentrates (CFC) on the glycocalyx in hemorrhagic shock (HS). We hypothesized that colloid-based resuscitation supplemented with CFCs offers a therapeutic value to treat endothelial damage following HS. Eighty-four rats were subjected to pressure-controlled (mean arterial pressure (MAP) 30-35 mm Hg) and lab-guided (targeted cutoff: lactate >2.2. mmol/L and base deficit > 5.5 mmol/L) HS. Animals were resuscitated with fresh frozen plasma (FFP), human albumin (HA) or Ringer's lactate (RL) and RL or HA supplemented with fibrinogen concentrate (FC) or prothrombin complex concentrate (PCC). Serum epinephrine and the following markers of endothelial damage were assessed at baseline and at the end-of-observation (120 min after shock was terminated): syndecan-1, heparan sulfate, and soluble vascular endothelial growth factor receptor 1 (sVEGFR 1). Resuscitation with FFP had no effect on sVEGFR1 compared with crystalloid-based resuscitation (FFP: 19.3 ng/mL vs. RL: 15.9 ng/mL; RL+FC: 19.7 ng/mL; RL+PCC: 18.9 ng/mL; n.s.). At the end-of-observation, syndecan-1 was similar among all groups. Interestingly, HA+FC treated animals displayed the highest syndecan-1 concentration (12.07 ng/mL). Resuscitation with FFP restored heparan sulfate back to baseline (baseline: 36 ng/mL vs. end-of-observation: 36 ng/mL). The current study revealed that plasma-based resuscitation normalized circulating heparan sulfate but not syndecan-1. Co-administration of CFC had no further effect on glycocalyx shedding suggesting a lack of its therapeutic potential. VExperimental in vivo study.

Colloid Oncotic Pressure in Children with Nephrotic Syndrome

To evaluate the correlation between plasma protein concentration and colloid oncotic pressure (COP) and their influence on clinical symptom of edema, we studied 30 children with nephrotic syndrome (NS). Total plasma protein concentration (TP), albumm, globulin and COP were measured in all patients in edema forming state (EF) and m steady state phase (SS), except for COP, only 16 samples in SS phase.
 COP TP plasma albumin and globulin contents in EF group were 8. 7 ± 2. 7 mmHg, 4.07 '± 0.68 g/dl; 2.57 ± 0.50 g/dl and 1.51 ± 0.32 g/dl, respectively. In SS group these figures rose significantly to 16.7 ± 3.9 mmHg for COP; 5. 70 ± 0.99 g/dl for TP; 3.46 ± 0.52 g!dl and 2.06 ± 0.56 g/dl for plasma albumin and globulin, respectively. We also found the high correlation both between COP and albumin content (r= +0.58; p < 0.01) and between COP and TP (r= +0.54; P < 0.01) .
 A strong negative correlation was also found between COP and the degree of edema (r = _ 0.55; p <0.01). On the other hand a very low grade correlation was noticed between plasma albumin content and the degree of edema (r= - 0.26; P < 0.05) and no correlation at all was found between edema and TP (r= - 0.19; P > 0.05).
 We conclude that COP has the highest correlation with plasma protein concentration and the degree of edema, and can be used as a diagnostic tool. It is even more sensitive and simple compared with the TP or albumin content determination.

Cardiovascular diseases during pregnancy and delivery

Nowadays, cardiovascular diseases are the leading cause of maternal morbidity and mortality in the current obstetric practice. PHYSIOLOGICALLY ADAPTED MECHANISMS OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY: It is normal that during pregnancy some physiological adaptive changes of the cardiovascular system occur and they may contribute to the deterioration of the clinical cardiac status of a patient with preexisting or acquired cardiovascular disease. The most prominent adaptive mechanisms include the increase of circulating blood volume, decrease of peripheral vascular resistance and decrease of plasma colloid-oncotic pressure. MOST FREQUENT DISEASES OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY: Due to these changes, pregnant women are prone to tachycardia, palpitations and peripheral edema. Maternal counseling is obligatory for each pregnant woman in order to decrease the maternal morbidity and mortality. The most important predictors of maternal mortality for pregnant women with cardiovascular diseases are severity of pulmonary hypertension, hemodynamic significance of valvular lesion, cyanosis and functional status in heart failure. Cardiovascular diseases in pregnant women may be congenital or acquired. The most frequent congenital cardiac diseases are atrial and ventricular septal defects as well as persistent ductus arteriosus. These diseases are mainly diagnosed and corrected before the pregnancy, or left untreated if hemodynamically insignificant. The most frequent acquired cardiovascular diseases during pregnancy include arrhythmias, ischemic heart disease, rheumatic mitral stenosis and insufficiency, arterial hypertension and aortic dissection. In all cases of pregnancy associated with cardiovascular diseases, early recognition of cardiovascular disease is crucial, as well as correct diagnosis and referral to a tertiary centre equipped for a multidisciplinary approach of specialists experienced in high-risk pregnancies and deliveries in order to prevent maternal mortality.

Effects of general anesthesia on plasma colloid oncotic pressure in dogs

To determine the magnitude of the change in colloid oncotic pressure (COP) associated with general anesthesia in dogs undergoing a variety of elective procedures. Cohort study. 50 client-owned dogs. For each dog, preanesthetic and postanesthetic PCV, plasma total solids (TS) concentration, and COP were determined. The procedures requiring anesthesia, volume of crystalloid fluids administered IV, duration of anesthesia, age, weight, and sex were recorded. Postanesthetic PCV (mean +/- SD, 41.8 +/- 5.4%), TS concentration (6.3 +/- 0.8 g/dL), and COP (19.4 +/- 3.6 mm Hg) were significantly decreased, compared with preanesthetic values (48.8 +/- 5.9%, 7.2 +/- 0.7 g/dL, and 24.4 +/- 4.2 mm Hg, respectively). None of the variables tested could be used to reliably predict changes in COP. Results suggested that COP in healthy dogs may decrease by 5 mm Hg on average after general anesthesia and that this decrease may not be reliably predicted by the volume of fluids administered IV during anesthesia or by the concurrent measured decrease in TS concentration.

Clinical use of albumin in hepatology.

Albumin has been the subject of much discussion and research for a long time. Hippocrates first mentioned some of its physiological properties, but albumin was not named or studied until the early 1800s. The modern use of human albumin was established during World War II due to the demand for plasma substitutes, while the first documented clinical use of human albumin occurred in 1941 in seven sailors severely burned during the attack at Pearl Harbour. The first report of administration of albumin to patients with cirrhosis was published by Janeway et al., who treated six patients with cirrhosis with 25 g albumin per day1. This protein was introduced as a treatment in the 1950s and was incorporated for many years in the management of patients with decompensated cirrhosis. There were, however, always varied opinions among hepatologists in relation to the use of albumin in liver cirrhosis. This review aims to highlight current thinking regarding albumin therapy in the setting of hepatology and also discusses its potential therapeutic applications based on the complex biochemistry of this multifunctional plasma protein. Properties and physiological functions of albumin Human serum albumin is an abundant multifunctional non-glycosylated, negatively charged plasma protein, which is synthesised primarily in the liver and is thought to be a negative acute-phase protein2. In healthy adults, albumin synthesis occurs predominantly in polysomes of hepatocytes (10–15 g/day) and accounts for 10% of total liver protein synthesis. Relatively small amounts of albumin are hepatologically stored (<2 g), the majority being released into the vascular space. Approximately 30%–40% of the albumin synthesised is retained within the plasma compartment. The remaining pool is located in tissues such as muscle and skin. Albumin is not stored hepatically and there is, therefore, no reserve for release on demand3. However, under physiological circumstances only 20–30% of hepatocytes produce albumin and synthesis can, therefore, be increased on demand by 200–300%. Synthesis is a constant process, regulated at both transcriptional and post-transcriptional levels by specific stimuli, but a change in interstitial colloid oncotic pressure is thought to be the predominant regulatory influence4. Albumin homeostasis is maintained by balanced catabolism occurring in all tissues, with most albumin (40%–60%) being degraded in muscles, the liver, and the kidneys. Studies of radiolabelled albumin catabolism in normal healthy young adult males indicate that the protein has a mean half-life of 14.8 days5. Colloid oncotic pressure Human serum albumin accounts for some 60% of the intravascular protein pool in healthy individuals, thereby being responsible for approximately 60% of plasma colloid oncotic pressure. Albumin is also responsible for water retention as the negative charges surrounding the protein molecules attract sodium ions. Its remaining contribution to colloid oncotic pressure is due to the Gibbs-Donnan effect of attracting other active positive ions, further enhancing its water-retaining effect6. In patients with hypoalbuminaemia (especially when it is associated with inflammation or sepsis) whose capillaries are known to be hyperpermeable, the leakage of albumin into the interstitial space draws water with it, producing oedema. Moreover, albumin may influence vascular integrity both directly, by binding in the interstitial matrix and subendothelium and reducing the permeability of these layers to large molecules, and indirectly, through its scavenging properties.

Neurogenic pulmonary oedema post-haemodialysis.

Pulmonary oedema can develop due to many causes (Table 1). In the patient with renal failure, pulmonary oedema typically occurs in the setting of raised pulmonary arterial pressure due to extracellular fluid expansion, due to a combination of excessive inter-dialytic weight gain and failure to achieve ‘dry’ or ‘post-dialysis target’ weight, often associated with cardiac dysfunction. However, increased lung interstitial fluid can also occur in conditions, typified by normal pulmonary arterial pressures. Pulmonary complications are well recognized in both acute and chronic liver failure. Excessive pulmonary vasodilatation, in combination with high levels of vasopressin, catecholamines and sympathetic nervous system activity, leads to shunting, with increased V/Q mismatch, termed the hepatopulmonary syndrome [1]. In addition, increased circulating endotoxin and pro-inflammatory cytokines lead to increased pulmonary endothelial activation and increased pulmonary interstitial fluid formation [2]. This can be exacerbated by a concomitant reduction in plasma colloid oncotic pressure. In cases of neurogenic pulmonary oedema, pulmonary hydrostatic pressure and endothelial activation combine to increase lung interstitial water [3]. A case of acute pulmonary oedema occurring after intermittent haemodialysis treatment is reported in a patient, 9 days after paracetamol (acetaminophen) self-poisoning, due to neurogenic pulmonary oedema.

Beneficial effects of recombinant human activated protein C in a ewe model of septic shock*

To investigate the effects of activated protein C (APC) in a clinically relevant animal model of septic shock. Prospective, randomized, controlled study. University medical center research laboratory. Eighteen female sheep (body weight, 27-35 kg). Animals were fasted, anesthetized, invasively monitored, and mechanically ventilated before receiving 0.5 g/kg body weight of feces intraperitoneally to induce sepsis. Fluid resuscitation with Ringer lactate was titrated to maintain pulmonary artery occlusion pressure at baseline levels. No vasoactive agents or antibiotics were used. Two hours after the induction of sepsis, animals were randomized to receive an infusion of APC (24 microg x kg(-1) x hr(-1), n = 9) or an equivalent volume of vehicle (n = 9) throughout the experimental period. The APC-treated animals had significantly higher arterial pressure, urine output, PaO2/FIO2 ratios, and thoracopulmonary compliance than the control animals. They had lower pulmonary arterial pressure and arterial lactate concentrations than the control animals. Plasma colloid oncotic pressure was better maintained in the APC-treated group than in the control group (p < .05). Prothrombin time and activated partial thromboplastin time were altered less, and plasma D-dimer concentrations were significantly lower in the APC-treated group than in the control group (p < .05). The blood protein C concentration and platelet count were maintained better in the APC-treated group than in the control group (p < .05). APC administration was associated with significantly longer survival (median, 27 hrs vs. 20 hrs; p < .05). At postmortem examination, the lung wet/dry ratio was significantly lower in the APC group than in the control group (6.3 +/- 0.7 vs. 7.1 +/- 1.2, p < .05). In this clinically relevant model of septic shock due to fecal peritonitis, administration of APC had beneficial effects on hemodynamic variables, gas exchange, lactic acidosis, and coagulation abnormalities. Higher colloid oncotic pressures and lower lung wet/dry ratios at autopsy suggest preserved endothelial integrity. APC administration resulted in prolonged survival.

Blood viscosity in patients with bone fractures and long term bedrest.

Eighteen patients with bone fractures and without systemic disease were studied for blood rheology. Blood and plasma viscosities, haematocrit, red cell aggregation and filterability as well as plasma colloid oncotic pressure were measured. Results show that patients exhibit a substantial haemorheological deficit on admission. During bedrest this returns to normal, owing to marked 'autohaemodilution'. It is concluded that trauma causes increased viscosity of blood in these patients. This change could predispose to deep vein thrombosis. However, such a risk is reduced by 'autohaemodilution' which is most probably an effect of immobilization.

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.

Diffusion-weighted magnetic resonance imaging confirms marked neuroprotective efficacy of albumin therapy in focal cerebral ischemia.

We have recently shown high-dose human serum albumin therapy to confer marked histological protection in experimental middle cerebral artery occlusion (MCAo). We have now used diffusion-weighted magnetic resonance imaging (DWI) in conjunction with morphological methods to expand our understanding of this therapeutic approach. Physiologically controlled Sprague-Dawley rats received 2-hour MCAo by the modified intraluminal suture method. Treated rats received 25% human serum albumin solution (1% by body weight) immediately after the MCA was reopened. Vehicle-treated rats received saline. Computer-based image averaging was used to analyze DWI data obtained 24 hours after MCAo and light-microscopic histopathology obtained at 3 days. In a matched series, plasma osmolality and colloid oncotic pressure, as well as brain water content, were determined. Albumin therapy, which lowered the hematocrit on average by 37% and raised plasma colloid oncotic pressure by 56%, improved the neurological score throughout the 3-day survival period. Within the ischemic focus, the apparent diffusion coefficient (ADC) computed from DWI data declined by 40% in vehicle-treated rats but was preserved at near-normal levels (8% decline) in albumin-treated rats (P<0.001). Albumin also led to higher ADC values within unlesioned brain regions. Histology revealed large consistent cortical and subcortical infarcts in vehicle-treated rats, while albumin therapy reduced infarct volume at these sites, on average, by 84% and 33%, respectively. Total infarct volume was reduced by 66% and brain swelling was virtually eliminated by albumin treatment. Microscopically, while infarcted regions of vehicle-treated rats had the typical changes of pannecrosis, infarcted zones of albumin-treated brains showed persistence of vascular endothelium and prominent microglial activation, suggesting that albumin therapy may help to preserve the neuropil within zones of residual infarction. These findings confirm the striking neuroprotective efficacy of albumin therapy in focal cerebral ischemia and reveal that this effect is associated with DWI normalization and a mitigation of pannecrotic changes within zones of residual injury.

Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis

Increased VLDL in nephrotic patients results from a decreased catabolism while increased LDL results from increased synthesis

Application of Polygeline in Pediatric Cardiac Surgery

The purpose of this study was to determine the effect of using polygeline as part of the cardiopulmonary bypass solution in pediatric cardiac surgery. A total of 40 cases were divided into two groups, a polygeline group (H group, n=20) and a plasma group (P group, n=20). Operations were performed under routine extracorporeal circulation. The dose of polygeline or plasma used was calculated to maintain the patient's plasma colloid oncotic pressure at 10-12 mmHg. The results showed that in the polygeline group, no patient developed allergic or coagulation disorders even after large volumes of polygeline were used (45 ml/kg). At the initiation and completion of cardiopulmonary bypass (CPB), the concentrations of calcium were higher in the H group (1.38 ± 0.19, 1.21 ± 0.11) than those (0.72 ± 0.11, 0.95 ± 0.10) in the P group. There were no other statistically significant differences between the two groups. There were no organ problems in the patients included in the study. This study demonstrated that polygeline could be used as part of prime solution instead of plasma to keep an ideal plasma colloid oncotic pressure, reduce infections caused by blood product transfusions and lower the cost to the patients.

Effect of Synthetic Colloids on Refractometric Readings of Total Solids

SummaryVeterinary patients are treated with colloid solutions for plasma volume expansion and maintenance of plasma colloid oncotic pressure (COP). In practice COP is usually extrapolated from measurement of albumin, total protein, or refractometric total solids (TS) as an estimate of total protein. The objective of this study was to determine if refractometer readings accurately reflect levels of synthetic colloid in the blood. Serial dilutions of synthetic colloids Dextran 70 and hetastarch into 2.5% and 5% human serum albumin (HSA) were prepared, and COP and TS measurements were performed. Synthetic colloids were found to produce a significant increase in measured COP, without a significant change in refractometric TS readings. Measured COP correlated well with concentration of synthetic colloid. In clinical patients, treatment of decreased COP with synthetic colloids should be monitored by direct measurement of COP or by observing resolution of clinical signs of hypovolemia or edema. (Vet Emerg &amp; Crit Care, 1998; 8: 21–26)

Long-term high-colloid oncotic therapy for ischemic brain edema in gerbils.

We evaluated the effects of long-term administration of high-colloid oncotic pressure on ischemic brain edema in Mongolian gerbils. Animals that exhibited stroke after 35 minutes of unilateral forebrain ischemia were used. The gerbils were divided into albumin- (1 g/kg body wt, 25% albumin; n = 30) and saline-injected (4 mL/kg; n = 30) groups. Both agents were administered intravenously every 12 hours starting immediately after the recirculation. Plasma colloid oncotic pressure, serum sodium and potassium concentrations, and brain water, sodium, and potassium content were measured 24, 48, and 72 hours after recirculation. Plasma colloid oncotic pressure at 24, 48, and 72 hours after recirculation was significantly higher in the albumin- (26.1 +/- 2.3 mm Hg) than in the saline-treated group (18.5 +/- 1.9 mm Hg; P < .01), and brain water content of the ischemic hemisphere was significantly lower in the albumin group (79.5%, 80.2%, and 80.5%, respectively) than in the saline group (80.9%, 81.6%, and 82.1%, respectively; P < .05) at all three time points. Brain sodium content at 24 hours was significantly lower in the albumin than in the saline group (P < .05), while brain potassium content at 24 and 48 hours was significantly higher in the albumin than in the saline group (P < .05). The changes in brain water and sodium plus potassium content, which were calculated from differences between the ischemic and nonischemic hemispheres, showed a significant correlation in both groups (P < .01), but there was no significant difference between the linear regression lines for both groups. Long-term high-colloid oncotic pressure was effective in treating ischemic brain edema, probably acting by diminishing the bulk flow through the disrupted blood-brain barrier and ameliorating the vasogenic edema.

Hematological alterations after acute exposure to hyperbaric oxygen in rats.

1. Acute exposure to hyperbaric oxygen (HBO) is associated with a significant increase in haematocrit which returns to the control level after 24h of recovery in room air. In this study we report changes in blood viscosity in Sprague-Dawley rats after acute exposure to HBO. 2. The rats were divided into three groups: a control group included rats not exposed to HBO (CON), a group studied immediately after acute exposure to HBO at 283.7 kPa for 6h (HBO), and a group allowed to recover for 24h in room air after HBO exposure (REC). 3. The viscosity of the whole blood, plasma and red blood cells (RBC) suspension was measured in the three groups. A significant increase in whole blood viscosity was detected in HBO and REC groups compared with CON (P < 0.05), but no changes in the viscosity of the plasma or RBC suspension were noted. 4. A significant decrease in oxygen delivery index was found in the REC group compared with the CON and HBO groups (P < 0.05). 5. In a subgroup of rats, several blood parameters known to influence blood viscosity were evaluated. A significant increase in plasma colloid oncotic pressure was noted in HBO rats compared with CON (P < 0.01). A marked increase in platelet count and fibrinogen concentration was detected in HBO and REC rats compared with CON (P < 0.05). Furthermore, a significant increase in total leukocytic count was noticed in REC group compared with CON and HBO (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the pressure-flow characteristics of isolated perfused rat kidneys with inhibited tubular reabsorption.

The renal hemodynamics were studied in an isolated perfused rat kidney model modified for investigations of the glomerular permeability characteristics. The tubular reabsorptive activity was inhibited by perfusion at low temperature (8 degrees C) in the presence of furosemide and nitroprusside resulting in a dramatic increase in the filtered load of fluid and solute reaching the tubules and hence in tubular pressure. The glomerular filtration rate (GFR), arterial pressure (PA) and needle pressure (intrarenal tissue pressure, PiR) were continuously recorded and the glomerular hydrostatic pressure was estimated by an arterial occlusion technique. The pre- to postglomerular resistance ratio was calculated from the pressure vs. GFR relationships for two perfusates having differing oncotic pressures (pi = 5.5 and pi = 20 mmHg), from which estimations of glomerular hydrostatic pressures (PGC) were concomitantly made. Thus, increases in delta pi could be exactly counterbalanced by equally large increases in PGC for any given GFR, the needle and Bowman's capsule pressures being dependent on GFR but not on plasma colloid oncotic pressure. The experimental interventions resulted in a pronounced elevation of PiR as compared with in vivo conditions, while the PGC values were in a normal range, resulting in reduced glomerular filtration pressures. Furthermore, the clearance of albumin varied with the oncotic pressure in agreement with the notion of heteroporosity.

Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.

Hemodynamics of Preeclampsia

A review of the English literature reveals considerable disagreement regarding the cardiovascular hemodynamics of preeclampsia as measured by both noninvasive and invasive techniques. In the untreated patient, most of the data suggest the presence of low CO, low PCWP, and elevated SVR as compared to normotensive pregnancy. In contrast, in patients receiving treatment prior to the measurements, the majority of the data indicate the presence of normal to elevated CO, PCWP, and SVR. There is general agreement that plasma colloid oncotic pressure is markedly reduced in patients with severe disease, and this reduction is more dramatic in the postpartum period especially in those receiving excessive crystalloid therapy. As a result, these patients are at increased risk for pulmonary edema. Several studies recommended using plasma and plasma substitutes to correct the reduced plasma volume and PCWP prior to the use of vasodilator therapy in such pregnancies. This management requires the use of invasive hemodynamic monitoring, and its benefit is transient and not well established. Finally, the true cardiovascular hemodynamics of preeclampsia remain unknown.