Plasma adrenaline and noradrenaline during mental stress and isometric exercise in man. The role of arterial sampling

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during isometric exercise and during a mental stress test. In both conditions arterial plasma adrenaline increased significantly, whereas arterial plasma noradrenaline remained unchanged. During isometric exercise the increase in plasma adrenaline was greater in venous blood from the exercising arm than from the resting arm. The extraction of adrenaline in the forearm was greater in the resting than in the exercising arm. Venous plasma noradrenaline showed a rebound phenomenon after isometric exercise and tended to decrease during the mental stress test. The results indicate that it is preferable to measure arterial concentrations of adrenaline as an indicator of sympathoadrenal activity rather than venous concentrations since the extraction of adrenaline in forearm might not be constant. It is suggested that a selective increase in arterial plasma adrenaline as opposed to an increase in both plasma adrenaline and noradrenaline may indicate a selective increase in sympathoadrenal activity in visceral organs.     

Concentration of serum prealbumin and retinol-binding proteins during pregnancy

Concentrations of the rapid-turnover plasma proteins prealbumin and retinol-binding protein are measured in nonpregnant subjects to detect subclinical malnutrition. In this study, blood samples were taken from 30 normal pregnant women to establish normative data on the concentrations of these two plasma proteins during pregnancy. Twenty-five normal adults were used as controls. Total protein and albumin were concomitantly measured and, as expected, the concentration of both decreased during pregnancy. In contrast, plasma concentrations of prealbumin and retinol-binding protein remained unchanged. Two malnourished pregnant women had low levels of both prealbumin and retinol-binding protein, which reverted to normal once adequate caloric and protein intake was established. These findings suggest that prealbumin and retinol-binding protein measurements may be used during pregnancy to detect malnutrition and monitor the effect of dietary therapy.     

Corticosteroid binding globulin in normotensive and hypertensive human pregnancy

Corticosteroid binding globulin (CBG) concentrations in maternal plasma have been measured throughout pregnancy in a series of 100 singleton pregnancies in 89 normotensive women. Plasma CBG concentrations were monitored also in 10 women with essential or renovascular hypertension. Plasma albumin, cortisol and oestriol were measured concurrently. Plasma CBG increased two and a half to three times during pregnancy. In those women who developed hypertension in pregnancy (mean arterial pressure greater than 107 mmHg), the plasma CBG concentrations were significantly lower than in those who remained normotensive. In women who developed hypertension, the CBG either failed to increase at the same rate as in normal pregnancies or the level fell before the appearance of hypertension. The earlier the onset of hypertension, the greater the decline in CBG. In all subjects, the CBG concentration at 34-36 weeks gestation was directly related to the birthweight of the infant. Plasma cortisol levels were depressed in hypertension relative to that in the normotensive women. Whilst plasma albumin levels decreased at least 30% in most women during pregnancy, the fall tended to be less in hypertensive women, but there was marked overlap between patient groups. Plasma oestriol concentrations were depressed only in the very severely affected cases. It is suggested the CBG concentration is a further reflection of the metabolic abnormalities associated with hypertension in pregnancy, and that it can be used as a marker to identify and monitor those patients at risk.     

Intraplatelet serotonin in patients with diabetes mellitus and peripheral vascular disease

Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. Intraplatelet 5-HT content in normal subjects showed an age-related decline (r = -0.45; P less than 0.008), as has been previously demonstrated. The median 5-HT content in platelets of the young normal subjects was 4.36 (range: 3.62-6.79) nmol 10(-9) platelets, while that in the elderly normal subjects was 3.87 (range: 2.8-6.0) nmol 10(-9) platelets and that in young + elderly subjects was 4.05 (range: 2.8-6.8) nmol 10(-9) platelets. The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. The presence of hypertension in DM patients caused a small but significant (P less than 0.05) decrease in intraplatelet 5-HT content, whilst its presence had no effect in PVD patients. In a smaller study, it was established that NIDDM and PVD patients have significantly (P less than 0.002) greater plasma 5-HT concentrations than controls. Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enhanced urinary excretion of albumin in congestive heart failure: effect of ACE-inhibition.

Urinary excretion of albumin and beta 2-microglobulin were measured in 13 patients with congestive heart failure, NYHA class II-IV, before and after captopril treatment for 4 weeks, and in 13 healthy control subjects. The urinary excretion of albumin was enhanced in heart failure patients compared to control subjects (12.0 micrograms min-1 vs 2.8 micrograms min-1; medians, p less than 0.01), whereas beta 2-microglobulin excretion was normal. No significant change in urinary excretion of albumin was observed after captopril. Using Spearmann's test the urinary excretion of albumin was correlated to the NYHA class (Px = 0.681, p less than 0.05, plasma renin (Px = 0.886, p less than 0.01) and plasma angiotensin II (Px = 0.5840, p less than 0.05). Correlations with atrial natriuretic peptide (rho = 0.412, p = 0.153) and aldosterone (Px = 0.487, p = 0.106) did not reach significance. By multiple linear regression analysis only plasma renin activity was correlated to albumin excretion. In conclusion, patients with congestive heart failure had an increased urinary excretion of albumin. It is suggested that the enhanced transglomerular passage of albumin in congestive heart failure is partly due to an increased intra-renal angiotensin II generation, but elevated plasma level of atrial natriuretic peptide and increased renal venous pressure may also be important pathogenetic factors.     

The effect of glycemic control on plasma soluble fibrin monomer complexes and fibronectin in diabetic patients

We have shown previously that increased concentrations of plasma soluble fibrin monomer complexes (SFMC) and elevated fibronectin (Fn) levels are closely related to the development of diabetic microangiopathy. The purpose of the present study was to explore whether or not changes in plasma glucose levels could have an effect on these protein constituents. Plasma glucose levels of 25 uncontrolled diabetic patients were brought under control with insulin and serial measurements of SFMC and Fn were made over a period of 4 weeks. Glucose values fell from an average of 312 mg/100 ml to 160 mg/100 ml. Ten patients with macroproteinuria (i.e. greater than or equal to 0.5 g/24 hr) showed initially elevated plasma SFMC and Fn concentrations. These levels fell significantly over the 4 week observation period: from 13.6 mg/100 ml to 9.4 mg/100 ml for SFMC and from 38.4 mg/100 ml to 34.5 mg/100 ml for Fn. The remaining 15 patients had nearly normal levels of both SFMC (7.9 mg/100 ml) and Fn (31.1 mg/100 ml) and glycemic control brought no further reduction. The data indicated that a) elevated SFMC and Fn levels are indeed associated with diabetic microangiopathy, especially in the presence of macroproteinuria; and b) adequate glycemic control is capable of normalizing the plasma concentration of these constituents.     

THE CONCENTRATION OF THE PLASMA PROTEINS IN NEPHRITIS

In nephrosclerosis (Volhard and Fahr classification of nephritis) there was no decrease in the plasma proteins. With heart failure the ratio of albumin to globulin fell from the normal 1.7 ± 0.3 to about 1. There is a sharp difference between the two types of glomerulonephritis in the effect on plasma proteins. In the vascular-interstitial type the effect was the same as in nephrosclerosis. There was no decrease in the plasma proteins until shortly before death. In the glomerulotubular or nephrotic type, active or recently active, the total plasma proteins were less than 5 gm. per 100 cc. This decrease from the normal 5.5 to 7.5 occurred whether edema was present or absent. The decrease affected chiefly the albumin, the globulin being usually diminished but little, and sometimes slightly increased. Consequently the ratio of albumin to globulin was reduced to less than 1, and occasionally to 0.6. In nephrosis similar changes were found in the total protein concentration but in severe cases the decrease in albumin was greater than in nephrotic glomerulonephritis while the globulin was either very slightly reduced or was increased. The albumin : globulin ratio was therefore lower than in nephrotic glomerulonephritis, ranging down to 0.26. With the disappearance of edema there was usually an increase in the plasma protein concentration, but this was not invariable, and concentrations of 4.5 per cent or less were compatible with the persistent absence of edema. The ratio of albumin to globulin showed an irregular tendency to rise. Whenever the total concentration was less than 4 per cent there was some edema present, but it was sometimes slight in amount. With recovery in acute cases, and remission with decrease of proteinuria in chronic cases, normal concentrations were regained. The albumin : globulin ratio remained low in some instances for a longer period on account of an absolute increase in globulin concentration. In "functional proteinuria" no change in plasma proteins was found. Low plasma protein concentrations were always associated with considerable losses of protein in the urine, but these losses did not provide an explanation for all our observations. A disturbance in the production of the plasma proteins appears probable.     

Changes in the concentrations of hydroxyproline, glycine and serine in the plasma of haemodialysis patients undergoing erythropoietin therapy

The concentrations of proline, hydroxyproline, glycine and serine were determined in the plasma of 39 haemodialysis patients and 18 healthy subjects, using liquid chromatography with fluorescence detection. Plasma concentrations of the N-terminal immunoreactive parathyrin were also measured. In haemodialysis patients, the plasma concentrations of glycine (p less than 0.01), hydroxyproline (p less than 0.05) and proline (p less than 0.10) were significantly increased, whereas the serine concentrations (p less than 0.01) were decreased, compared with those of the healthy controls. Haemodialysis patients showed greatly elevated plasma N-terminal immunoreactive parathyrin values (greater than 30 pmol/l), which showed a significant correlation with the hydroxyproline values (r = 0.79). Fourteen haemodialysis patients received erythropoietin therapy. In these patients, changes in the concentrations of plasma amino acids were observed up to one year after the beginning of therapy. In the course of the erythropoietin therapy, the plasma concentrations of glycine (p less than 0.05) and hydroxyproline (p less than 0.10) of the haemodialysis patients decreased, whereas the concentration of serine increased (p less than 0.05) to approximately normal values. The results indicate that erythropoietin therapy leads to a normalization of amino acid metabolism.     

Measurement of acetate in human blood by gas chromatography: effects of sample preparation, feeding, and various diseases.

We measured acetate concentrations in whole blood, serum, and plasma by a modification of a previously described method involving vacuum distillation and gas chromatography. The mean acetate concentration of fresh venous plasma from 27 normal subjects was 51 +/- 5 mumol/L (95% confidence limits ranged from 0 to 103 mumol/L). The acetate concentrations of serum and plasma incubated for 2 h at either 4 degrees C or 27 degrees C were the same. The acetate concentration of whole blood incubated at 27 degrees C was significantly greater than that of blood incubated at 4 degrees C. This change may have resulted from the production of acetate by erythrocytes or from the hydrolysis of acetate esters. Storage of plasma at -20 degrees C for 24 h significantly increased acetate concentrations from 26 +/- 6 mumol/L to 63 +/- 4 mumol/L. After the subjects consumed a standard breakfast, venous plasma acetate concentrations increased from 58 to 97 mumol/L at 30 min. Acetate concentrations in arterial plasma exceeded those in venous plasma. Plasma acetate concentrations were not significantly altered in patients with malignancy or diabetes mellitus, but severe liver disease and severe acidosis were both associated with increased acetate concentrations. These preliminary observations suggest that plasma acetate concentrations may be altered in several disease states.     

Complement activation and increased alveolar-capillary permeability after major surgery and in adult respiratory distress syndrome

The concentrations of C3a des Arg were measured in bronchoalveolar fluid (BAL) and plasma from 12 patients with adult respiratory distress syndrome (ARDS). Compared with 32 controls, all patients had increased BAL fluid levels (p less than .001), and nine of 12 had increased plasma levels (p less than .001) of this split product from the third complement component. Reduced total hemolytic activity (CH50) in serum was seen in five patients (p less than .01). As an indication of damage to the alveolar-capillary barrier, ten of the 12 ARDS patients had elevated albumin concentrations in BAL fluid (p less than .001). These signs of complement activation and lung tissue damage are not specific for ARDS. Thus, in 15 patients investigated preoperatively and postoperatively, we found that major surgery induced a significant increase of BAL fluid C3a (p less than .01) and plasma C3a (p less than .02), a significant reduction of CH50 (p less than .001), and a significant increase of BAL fluid albumin (p less than .02). Similar values of CH50 and plasma C3a were seen in ARDS and after surgery (p greater than .05). Of the 12 ARDS patients, eight had increased BAL fluid concentrations of C3a (p less than .001), and ten had increased BAL fluid levels of albumin (p less than .001) compared with the post-surgical patients. Measuring complement consumption in blood by these techniques is of limited value in ARDS due to the lack of specificity. BAL fluid albumin has a similar degree of sensitivity and specificity for ARDS as does BAL fluid C3a.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in calcium homoeostasis in patients undergoing liver transplantation: effects of a single infusion of pamidronate administered pre-operatively.

Bone turnover, bone loss and fracture risk increase after liver transplantation. It has been postulated that peri-operative administration of a bisphosphonate might prevent bone loss and reduce fracture rate. We studied the effects of a single pre-operative dose of pamidronate on biochemical parameters of skeletal metabolism in the first month after liver transplantation. In a randomized, single-blind study, six of 12 patients with chronic liver disease received 60 mg of pamidronate intravenously on a single occasion 1-30 days before transplantation. Six other patients undergoing transplantation received no pamidronate. We measured serum calcium, phosphate, albumin, bone-specific alkaline phosphatase, plasma parathyroid hormone and tartrate-resistant acid phosphatase before pamidronate infusion and at frequent intervals during the first 30 post-operative days. In treated patients, plasma parathyroid hormone increased 12-fold over baseline values and remained elevated in comparison with baseline at days 26-30; serum calcium and phosphate fell significantly, returning to normal at around day 14 post-operatively. There were no significant changes in any parameter in the untreated group. No changes in bone formation or resorption markers were observed in either group. The large increase in plasma parathyroid hormone concentrations in the treated group is probably secondary to the fall in serum calcium. The magnitude of the increase is much greater than that seen after pamidronate infusion in other patient groups. The lack of change in, or correlation of, serum calcium and plasma parathyroid hormone in the untreated group suggests that additional factors release calcium from bone after liver transplantation, presumably by increasing bone resorption.     

Protein losing enteropathy associated with Nippostrongylus brasiliensis infestation and its impact on albumin homoeostasis in rats fed two levels of dietary protein

Alterations in plasma albumin concentration and gastrointestinal permeability have been investigated in rats infected with the nematode Nippostrongylus brasiliensis and fed adequate or low protein diets. Infection caused only minor changes in growth and food consumption of well nourished rats but resulted in significant reductions in those fed the low protein diet. Animals in both dietary groups were able to mount an immune response beyond day 10 post-infection (p.i.) which caused expulsion of the parasites, but this was less effective in rats fed the low protein food. Uninfected rats fed the low protein diet had significantly lower plasma albumin concentrations than their well nourished counterparts. Animals of both dietary groups showed a progressive reduction in plasma albumin concentration as the infection developed but values returned towards normal as the parasites were expelled. The reduction in plasma albumin concentration was closely associated with increases in gastrointestinal leakage of plasma protein but losses were far greater in the protein deficiency animals. Beyond day 10 p.i. protein loss decreased in both dietary groups and by day 21 p.i. had returned to normal in well nourished animals but not those fed the low protein diet. Intestinal permeability measured by the lactulose:mannitol ratio technique gave similar results to the protein loss data. Permeability increased as the infection progressed then fell as the worms were expelled but remained above control values in infected protein deficient animals. Overall, animals fed the low protein diet were more severely affected by the parasite than were their well fed counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)     

Albumin metabolism in fasted subjects during late pregnancy.

1. Albumin fractional synthetic rate was determined in five non-pregnant subjects and five normal pregnant subjects in late gestation after an overnight fast by simultaneous prime and intravenous infusion of two precursor amino acids, [15N]glycine and L-[1-13C]leucine, with additional priming of the large but, slowly turning over, urea pool with [15N2]urea. 2. The two tracers yielded similar values of albumin fractional synthetic rate: 6.1 and 6.0%/day in non-pregnant subjects and 7.3 and 7.6%/day in pregnant subjects, for glycine and leucine, respectively. While plasma volume was greater and serum albumin concentration was significantly reduced during pregnancy, the calculated intravascular albumin mass was significantly increased in pregnant subjects. 3. The amount of albumin synthesized in the intravascular compartment was significantly greater at 8.8 and 9.5 g/day in pregnant subjects compared with 6.4 and 6.3 g/day in non-pregnant control subjects (glycine and leucine methods, respectively). Calculated whole-body protein turnover using glycine was not different between the two subject groups, but leucine flux was higher in pregnant subjects. Partitioning of nitrogenous products in urine revealed that pregnant subjects excreted less urea, less ammonia and less creatinine than the non-pregnant control subjects. 4. These findings suggest that whereas the serum albumin concentration decreases during pregnancy secondary to the large increase in plasma volume, there is an increase in albumin synthesis such that total intravascular albumin mass is increased in late pregnancy.     

The effect of synthetic very low calorie diets on the GH-IGF-1 axis in obese subjects

IGF-1 concentrations were measured in plasma from 20 obese patients and 20 age- and sex-matched control subjects all of whom were fasting. Plasma IGF-1 concentrations were lower (p less than 0.05) in the obese individuals than in the controls. Plasma GH and insulin responses to stimulation with oral glucose were measured in 7 healthy normal weight individuals and both before and after energy restriction in 7 obese individuals. Before treatment the obese individuals were hyperinsulinaemic (fasting and integrated stimulated concentrations p less than 0.05) and showed attenuation of the plasma GH response to stimulation (peak and integrated stimulated values p less than 0.05 and less than 0.005, respectively) following oral glucose when compared to normal weight controls. Plasma insulin levels fell (both fasting and integrated concentrations p less than 0.05 and less than 0.005, respectively) and stimulated plasma GH responses increased (both peak and integrated values p less than 0.01 and less than 0.05, respectively) in the obese individuals following 3 wk treatment with a synthetic very low energy diet. Plasma IGF-1 concentrations remained unchanged during energy restriction. These results fail to support an endocrine IGF-1 mediated feedback inhibition on the hypothalamic-pituitary axis as the cause of the attenuated release of GH in obesity.     

Reduced binding of added zinc in serum of patients with decompensated hepatic cirrhosis

Binding of zinc to macromolecules when added to serum was measured by ultrafiltration. At a final ratio of 0.6 mol zinc per mol albumin, zinc dissociable by glycine was significantly greater in diluted serum from patients with decompensated alcoholic cirrhosis than in normal serum samples similarly prepared. Low serum zinc concentrations, often observed in patients with alcoholic cirrhosis, may be related in part to a reduced affinity of plasma albumin for exchangeable zinc.     

Elevated plasma levels of adrenomedullin in congenital cyanotic heart disease.

Adrenomedullin is a novel hypotensive peptide originally isolated from human pheochromocytoma. Accumulating evidence suggests the possible involvement of adrenomedullin in the physiology of the pulmonary circulation and the pathophysiology of hypoxaemia. The aim of the present study was to investigate the pathophysiological significance of adrenomedullin in hypoxaemia caused by congenital cyanotic heart disease. Subjects were 16 patients with congenital cyanotic heart disease aged 0.8-10 years (Group C) and 12 age-matched control subjects (patients with coronary artery dilatation after Kawasaki disease; Group N). Plasma adrenomedullin concentrations were measured, using radioimmunoassay, in femoral venous, pulmonary arterial and pulmonary venous blood obtained during cardiac catheterization. Plasma adrenomedullin concentrations in Group C were significantly (3-fold) higher than those in Group N at all sampling sites. In Group C, plasma adrenomedullin concentrations in pulmonary venous blood were significantly lower than those in pulmonary arterial blood. Pulmonary uptake of adrenomedullin in Group C was significantly greater than that in Group N. Patients with congenital cyanotic heart disease showed elevated plasma adrenomedullin concentrations and an increased uptake of adrenomedullin in the pulmonary circulation, which may act to dilate pulmonary vessels and increase pulmonary blood flow to alleviate hypoxaemia. Intrinsically increased adrenomedullin levels may function as a compensatory mechanism for hypoxaemia in congenital cyanotic heart disease.     

Plasma fibronectin levels in sepsis: influencing factors

Low plasma levels of the opsonic glycoprotein fibronectin (Fn) have been suggested to imply an impaired host defense against sepsis. However, the mechanism(s) behind Fn depletion in sepsis are obscure. We measured the Fn plasma concentration in 32 patients 12 to 24 h after the diagnosis of septic shock. Although the average plasma level was low (214 +/- 80 [SD] mg/L) compared to that of a reference material (p less than .001), the range was great (60 to 403 mg/L). A multivariate analysis of some possible influencing factors showed significant (p less than .01) positive correlations to the prothrombin level (r = .62) and the amount of insulin infused per 24 h (r = .63). The relationships to disseminated intravascular coagulation-related variables, hemodilution, and outcome were weak. Cryoprecipitate was infused into 16 patients; Fn levels increased by 52 +/- 18% of the expected increase. The most severely ill patients displayed the lowest rates of increase. The postinfusion decrease in Fn plasma concentration indicated that the plasma half-life of cryoprecipitate Fn was about 25 h. The results support the concept that decreased Fn synthesis, probably in the liver, is the major reason for Fn depletion in sepsis, rather than an increased rate of consumption.     

Protein Digestion in Human Intestine as Reflected in Luminal, Mucosal, and Plasma Amino Acid Concentrations after Meals

Normal human volunteers were intubated with either aspiration tubes or a biopsy capsule placed in the small intestine. The subjects were then fed a test meal containing 50 g of purified bovine serum albumin which served as the model dietary protein. Electrophoretic analysis of intestinal fluids showed that for at least 4 h the fed albumin was detectable in jejunal and ileal fluids. On separate occasions, subjects were fed the same meal without the protein. No protein was detected in intestinal fluids when the protein-free meal was fed. After the protein-rich meal, total concentrations of measured free and peptide amino acids rose from 3.21 to 29.29, and 15.94 to 117.97 mumol/ml, respectively, (P values < 0.02) in the jejunum. Similarly, total concentrations of measured free and peptide amino acids rose from 5.45 to 19.74, and 13.59 to 65.39, respectively, (P values < 0.05) in the ileum. In contrast, concentrations of free and peptide amino acids in intestinal fluids did not increase after the protein-free meal. While intracellular concentrations of amino acids in the jejunal mucosa did not show significant changes, plasma concentrations of each individual free amino acid were increased after the protein-rich meal and were either decreased or unaltered after the protein-free meal. The amino acid composition of the fed protein was reflected in the increases in intraluminal and plasma concentrations of individual amino acids after the protein-rich meal. It is concluded that after the ingestion of a test meal containing a substantial amount of protein which is within the usual range of dietary intake; (a) the exogenous protein is the principal source of the increased free and peptide amino acids in the intraluminal contents and in the plasma; (b) there are greater amounts of amino acids present as small peptides than in the free form in the gut lumen; (c) the ingested protein can be recovered as late as 4 h both in the jejunum and in the ileum.     

Antithrombin III in critically ill patients

To assess the role of antithrombin III (ATIII) in the thrombotic complications of acutely ill patients who suffered from septicemia or trauma, with or without evidence of acute lung injury, we measured the plasma concentration of ATIII-related antigen (ATIII:Ag) in 146 patients with acute lung injury and in 43 critically ill patients without lung injury. We found plasma ATIII:Ag levels of both groups of acutely ill patients to be significantly lower than those of normal subjects (n = 21). The plasma ATIII:Ag levels of patients with acute lung injury, however, were significantly higher than those without lung injury (P < .01). By separating post-trauma acutely ill patients with lung injury from those with septicemia, we noted that their plasma ATIII:Ag levels were identical to those of normal subjects despite activation of blood coagulation. This finding led us to examine ATIII functional activity (ATIII:Fn) and search for ATIII-enzyme(s) complexes in 46 patients with acute lung injury (30 patients with sepsis and 16 post-trauma patients) and in 12 acutely ill patients without lung injury (eight patients with sepsis and four post-trauma patients). These 58 patients were representative of the groups studied and had no evidence of hepatic or renal dysfunction. We found significantly reduced ATIII:Ag and ATIII:Fn in septic patients, with or without lung injury, as compared with the normal levels (P < .05). After trauma, patients with or without lung injury had normal ATIII:Ag, but the ATIII:Fn levels were disproportionately lower. Following trauma, the ATIII:Ag/ATIII:Fn ratio was significantly higher than in septicemia patients or in normal patients. Patients who died from septicemia and post-trauma had higher ATIII:Ag to ATIII:Fn ratios, while surviving patients had ATIII:Ag to ATIII:Fn ratios closer to normal. In addition, in all post-trauma or septicemia patients, there was evidence of ATIII-enzyme(s) complex formation by cross-immunoelectrophoresis despite ATIII levels and the presence or absence of acute lung injury. High ATIII:Ag to ATIII:Fn ratios and the presence of circulating ATIII:enzyme(s) complexes were associated with high mortality. The ATIII alterations, however, did not allow us to determine the presence of acute lung injury. The ATIII changes observed in our patients appeared to be primarily influenced by the differing pathways of blood activation that occurred in septicemia and trauma.     

Increased transcapillary escape rate of albumin in patients with cirrhosis of the liver

The transcapillary escape rate of albumin (TERalb), i.e. the fraction of intravascular mass of albumin that passes to the extravascular space per unit time, was determined from the disappearance of intravenously injected 125I-labelled human serum albumin during the first 60 min after injection in nine patients with cirrhosis of the liver. Six of the patients had ascites. The wedged hepatic venous pressure or splenic pulp pressure ranged from 20 to 30 mmHg, mean 26 mmHg. Plasma albumin concentration was low, but plasma volume was slightly enlarged, and thus the intravascular mass of albumin was only moderately reduced. The transcapillary escape rate of albumin was significantly elevated in all the cirrhotics, mean 10.2%/h, range 8.8 to 12.3%/h, in comparison to values for twenty-eight normal subjects 5.4%/h, range 3.5-7.2%/h. Our results can best be explained by increased filtration out of the vessels in the portal system, due to the increased portal venous pressure. The increased TERalb probably contributes to the formation of oedema and ascitic fluid.