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At least 127 records · Page 7Linked to original sources
PubMed1983

Homologous radio-immunoassay of human plasma dopamine-beta-hydroxylase: analysis of homospecific activity, circulating plasma pool and intergroup differences based on race, blood pressure and cardiac function.

We used a homologous human dopamine-beta-hydroxylase (DBH) radio-immunoassay (RIA) to explore reported differences in plasma DBH enzymatic activity among patient groups stratified for race, blood pressure and cardiac function, as well as to determine plasma immunoreactive DBH protein pool and the relative activity of the enzyme in plasma versus human chromaffin tissue storage vesicles. Plasma DBH activity was lower in patients with congestive heart failure than in control subjects (19.9 +/- 4.0 versus 34.4 +/- 5.9 iu/l, P less than 0.05), paralleled by lower immunoreactive plasma DBH protein concentration (3.50 +/- 0.73 versus 6.34 +/- 1.05 micrograms/ml, P less than 0.05). All subject groups had similar plasma DBH homospecific activity (plasma DBH enzymatic activity/immunoreactive plasma DBH protein), ranging from 5.03 +/- 0.28 to 5.84 +/- 0.44 iu/mg. For the entire subject group, there was a significant relationship between plasma DBH activity and plasma DBH immunoreactive protein (r = 0.89, n = 78, P less than 0.01) from which no subgroup deviated systematically. Black hypertensives had lower plasma DBH activity than white hypertensives (23.0 +/- 5.2 versus 42.9 +/- 4.8 iu/l, P less than 0.01), though their plasma DBH homospecific activities and activity/immunoreactive protein plots were indistinguishable. Total circulating plasma DBH pools were large (from 13.1 +/- 3.7 to 27.5 +/- 4.8 mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Unbound phenytoin plasma concentrations in patients comedicated with sodium valproate--the predictive value of plasma albumin concentration.

1. Phenytoin protein binding in epileptic patients on phenytoin as monotherapy has been compared with protein binding in patients treated with both phenytoin and sodium valproate. In addition the relative value of assayed total phenytoin plasma concentrations and assayed unbound phenytoin plasma concentrations and the value of predicted unbound phenytoin plasma concentrations in predicting phenytoin toxicity has been assessed. 2. The mean phenytoin unbound fraction for patients taking sodium valproate (0.122) was significantly greater than for those on monotherapy (0.082). 3. There were six episodes of clinical toxicity. In five toxic episodes the assayed unbound phenytoin plasma concentration was a better reflection of toxicity than the assayed total phenytoin plasma concentration, and four of these occurred in patients on sodium valproate. 4. Unbound phenytoin plasma concentrations were predicted from a single regression equation correlating all assayed total phenytoin plasma concentrations with assayed unbound phenytoin plasma concentrations, from two separate regression equations for each group of patients, and from the correlation between phenytoin protein binding and plasma albumin concentration. 5. The unbound phenytoin plasma concentrations predicted from the two regression equations were statistically no less effective than the assayed unbound phenytoin plasma concentrations in assessing toxicity. 6. Despite a correlation between plasma albumin concentrations and phenytoin protein binding, the use of albumin concentrations in predicting unbound phenytoin plasma concentrations appeared to be of little additional benefit.

Adult↗
PubMed2006

Matrix metalloproteinase-9 activity in plasma correlates with plasma and whole blood lead concentrations.

Matrix metalloproteinases (MMPs) are enzymes involved in the degradation of the extracellular matrix. MMP-2 and MMP-9 have been implicated in a variety of pathological conditions including cardiovascular and neoplastic diseases, and recent studies have shown that circulating concentrations of MMP-9 may be a marker helping in the diagnosis and prognosis of cardiovascular and neoplastic diseases. We investigated whether there is an association between plasma MMP-2 and MMP-9 activities and the concentrations of lead in whole blood (blood Pb) or plasma (plasma Pb) from 40 lead-exposed persons (22 men and 18 women). Plasma Pb was determined by inductively coupled plasma mass spectrometry (ICP-MS) and blood Pb by graphite furnace atomic absorption spectrometry (GF-AAS). Plasma MMP-2 and MMP-9 activities were measured by gelatin zymography. We found a significant correlation between pro-MMP-9 activity in plasma and blood Pb (r=0.454; P=0.003), and between pro-MMP-9 activity in plasma and plasma Pb (r=0.312; P=0.049). No significant correlations were found between blood Pb or plasma Pb and plasma MMP-2. The association between pro-MMP-9 activity in plasma and both blood Pb and plasma Pb concentrations suggests a mechanism through which low lead exposure may increase the susceptibility to cardiovascular and neoplastic diseases. A causal relationship, however, remains to be proved.

Adolescent↗
PubMed1999

Species differences in the proportion of plasma lipoprotein lipid carried by high-density lipoproteins influence the distribution of free and liposomal nystatin in human, dog, and rat plasma.

The objective of this study was an interspecies comparison of free nystatin (NYS) and liposomal NYS (Nyotran) distribution in plasma. NYS and liposomal NYS at concentrations of 5, 10, and 20 microg of NYS/ml were incubated in human, dog, and rat plasma for 5, 60, and 180 min at 37 degrees C. Following these incubations, plasma samples were separated into their high-density lipoprotein (HDL), triglyceride-rich lipoprotein, low-density lipoprotein, and lipoprotein-deficient plasma (LPDP) fractions by density-gradient ultracentrifugation, and each fraction was assayed for NYS by high-pressure liquid chromatography. Total plasma and lipoprotein cholesterol, triglyceride, and protein concentrations in each human, dog, or rat plasma sample were determined by enzymatic assays. When NYS and liposomal NYS were incubated in human, dog, or rat plasma, the majority of the NYS was recovered in the LPDP fraction. For the 5- and 60-min incubation times for all plasmas measured, a significantly greater percentage of NYS was recovered in the lipoprotein fraction (primarily HDL) following the incubation of liposomal NYS than following the incubation of NYS. There was a significant correlation between the lipoprotein lipid and protein profiles in human, dog, and rat plasmas and the distribution of NYS and liposomal NYS in plasma. In particular, differences in the proportion of plasma lipoprotein cholesterol, triglyceride, and apolar lipids (cholesteryl ester and triglycerides) carried by HDL influenced the distribution of NYS and liposomal NYS within plasmas of different species. These findings suggest that the distribution of NYS among plasma lipoproteins of different species is defined by the proportion of lipid carried by HDL, and this is possibly an important consideration when evaluating the pharmacokinetics, toxicities, and activities of these compounds following administration to different animal species.

Animals↗
PubMed2000

Stability of plasma human immunodeficiency virus load in VACUTAINER PPT plasma preparation tubes during overnight shipment.

VACUTAINER PPT plasma preparation tubes were evaluated to determine the effects of various handling and shipping conditions on plasma human immunodeficiency virus (HIV) load determinations. Plasmas obtained from PPT tubes stored and shipped under nine different conditions were compared to conventional EDTA tube plasmas stored at -70 degrees C within 2 h after phlebotomy. Compared to viral loads in frozen EDTA plasma, those in PPT tube plasma that was frozen immediately and either separated or shipped in situ were not significantly different. Viral loads in PPT tube plasma after storage for 6 h at either room temperature or 4 degrees C, followed by shipment at ambient temperature or on wet or dry ice, were not significantly different from baseline viral loads in EDTA or PPT plasma. The results of this study indicate that the HIV load in PPT tube plasma is equivalent to that in standard EDTA plasma. Plasma viral load is not affected by storage or shipment temperature when plasma is collected in PPT tubes. Furthermore, plasmas can be shipped in spun PPT tubes, and the tubes provide a safer and more convenient method for sample collection and transport than regular EDTA tubes.

Anticoagulants↗
PubMed1984

Mechanism of acute depletion of plasma fibronectin following thermal injury in rats. Appearance of a gelatinlike ligand in plasma.

Plasma fibronectin was depleted within 15 min following sublethal burn, followed by partial recovery at 8 h and complete restoration by 24 h in anesthetized rats. Radiolabeled 75Se-plasma fibronectin, injected intravenously before burn, was rapidly sequestered in burn skin as well as the liver. Fibronectin levels at 2 h postburn as detected by immunoassay vs. 75Se-plasma fibronectin indicated that more fibronectin was in the plasma than detected by electroimmunoassay. Crossed immunoelectrophoretic analysis of fibronectin in early postburn plasma demonstrated a reduced electrophoretic mobility of the fibronectin antigen. Addition of heparin or fibrin, both of which have affinity for fibronectin, to normal plasma was unable to reproduce this altered fibronectin electrophoretic pattern. In contrast, addition of gelatin or native collagen to normal plasma reproduced the abnormal electrophoretic pattern of fibronectin seen in burn plasma. Extracts of burned skin, but not extracts of normal skin, when added to normal plasma, elicited a similar altered electrophoretic pattern for fibronectin. By gel filtration, fibronectin in burn plasma had an apparent molecular weight approximately 40% greater than that observed in normal plasma. These data suggest the release into the blood of a gelatinlike ligand from burned skin, which complexes with plasma fibronectin. Thus, fibronectin deficiency acutely postburn appears mediated by (a) its accumulation at the site of burn injury; (b) its removal from the circulation by the liver; and (c) its presence in the plasma in a form that is less detectable by immunoassay.

Animals↗
PubMed1982

Time trend analysis of plasma unconjugated and sulfoconjugated estrone and 3 beta-delta 5-steroids in fetal and maternal sheep plasma in relation to spontaneous parturition at term.

Parturition in the sheep is preceded by a complex series of changes in both fetal and maternal plasma-steroid hormone concentrations. Using the chronically catheterized fetal sheep preparation, we measured unconjugated and sulfoconjugated pregnenolone, 17 alpha-hydroxypregnenolone, dehydroepiandrosterone, and estrone in fetal and maternal plasma over the final 20 days before spontaneous vaginal delivery at term. Where appropriate, third degree polynomial functions were fitted to the changing plasma hormone concentration profile. Fetal and maternal plasma pregnenolone and pregnenolone sulfate both fell from maximum values in the last 4 days of gestation. Fetal and maternal plasma estrone and estrone sulfate concentrations underwent a terminal rise over the last 4 days of gestation that was a mirror image of the fall in plasma pregnenolone and pregnenolone sulfate. Maternal 17 alpha-hydroxypregnenolone rose over the last 4 days of gestation. Fetal 17 alpha-hydroxypregnenolone, maternal and fetal plasma dehydroepiandrosterone sulfate, and fetal plasma dehydroepiandrosterone sulfate, and fetal plasma dehydroepiandrosterone showed no trend during the period of study. Maternal plasma dehydroepiandrosterone rose over the last 4 days of gestation. These results support the view that increased activity of placental 17 alpha-hydroxylase and 17-20-desmolase is responsible for the conversion of C-21 steroids to estrogens at term. delta 5-Steroids are present in very high plasma concentrations in fetal sheep plasma and may constitute a more important precursor pool for estrogen biosynthesis than does circulating plasma progesterone.

17-alpha-Hydroxypregnenolone↗
PubMed2004

Sustained reduction in plasma free fatty acid concentration improves insulin action without altering plasma adipocytokine levels in subjects with strong family history of type 2 diabetes.

To investigate the effect of a sustained (7-d) decrease in plasma free fatty acid (FFA) concentration in individuals genetically predisposed to develop type 2 diabetes mellitus (T2DM), we studied the effect of acipimox, a potent inhibitor of lipolysis, on insulin action and adipocytokine concentrations in eight normal glucose-tolerant subjects (aged 40 +/- 4 yr, body mass index 26.5 +/- 0.8 kg/m(2)) with at least two first-degree relatives with T2DM. Subjects received an oral glucose tolerance test (OGTT) and 120 min euglycemic insulin clamp (80 mU/m(2).min) with 3-[(3)H] glucose to quantitate rates of insulin-mediated whole-body glucose disposal (Rd) and endogenous (primarily hepatic) glucose production (EGP) before and after acipimox, 250 mg every 6 h for 7 d. Acipimox significantly reduced fasting plasma FFA (515 +/- 64 to 285 +/- 58 microm, P < 0.05) and mean plasma FFA during the OGTT (263 +/- 32 to 151 +/- 25 microm, P < 0.05); insulin-mediated suppression of plasma FFA concentration during the insulin clamp also was enhanced (162 +/- 18 to 120 +/- 15 microm, P < 0.10). Following acipimox, fasting plasma glucose (5.1 +/- 0.1 vs. 5.2 +/- 0.1 mm) did not change, whereas mean plasma glucose during the OGTT decreased (7.6 +/- 0.5 to 6.9 +/- 0.5 mm, P < 0.01) without change in mean plasma insulin concentration (402 +/- 90 to 444 +/- 102 pmol/liter). After acipimox Rd increased from 5.6 +/- 0.5 to 6.8 +/- 0.5 mg/kg.min (P < 0.01) due to an increase in insulin-stimulated nonoxidative glucose disposal (2.5 +/- 0.4 to 3.5 +/- 0.4 mg/kg.min, P < 0.05). The increment in Rd correlated closely with the decrement in fasting plasma FFA concentration (r = -0.80, P < 0.02). Basal EGP did not change after acipimox (1.9 +/- 0.1 vs. 2.0 +/- 0.1 mg/kg.min), but insulin-mediated suppression of EGP improved (0.22 +/- 0.09 to 0.01 +/- 0.01 mg/kg.min, P < 0.05). EGP during the insulin clamp correlated positively with the fasting plasma FFA concentration (r = 0.49, P = 0.06) and the mean plasma FFA concentration during the insulin clamp (r = 0.52, P < 0.05). Plasma adiponectin (7.1 +/- 1.0 to 7.2 +/- 1.1 microg/ml), resistin (4.0 +/- 0.3 to 3.8 +/- 0.3 ng/ml), IL-6 (1.4 +/- 0.3 to 1.6 +/- 0.4 pg/ml), and TNFalpha (2.3 +/- 0.3 to 2.4 +/- 0.3 pg/ml) did not change after acipimox treatment. We concluded that sustained reduction in plasma FFA concentration in subjects with a strong family history of T2DM increases peripheral (muscle) and hepatic insulin sensitivity without increasing adiponectin levels or altering the secretion of other adipocytokines by the adipocyte. These results suggest that lipotoxicity already is well established in individuals who are genetically predisposed to develop T2DM and that drugs that cause a sustained reduction in the elevated plasma FFA concentration may represent an effective modality for the prevention of T2DM in high-risk, genetically predisposed, normal glucose-tolerant individuals despite the lack of an effect on adipocytokine concentrations.

Adiponectin↗
PubMed1996

Relationship of plasma leptin to plasma insulin and adiposity in normal weight and overweight women: effects of dietary fat content and sustained weight loss.

Leptin, the product of the human homologue of the ob gene, which is defective in the obese (ob/ob) mouse, may be a humoral regulator of human adiposity. Plasma leptin concentrations were measured by RIA in 19 normal weight [body mass index (BMI) = 24.5 +/- 0.6 kg/m2] and 19 overweight to obese (BMI = 34.7 +/- 1.2 kg/m2) nondiabetic postmenopausal women on sequential controlled weight-maintaining diets containing 31%, 23%, and 14% of energy as fat, each for 4-6 weeks. Thereafter, the subjects ate a very low fat diet (< 15%) ad libitum; plasma leptin and insulin concentrations, BMI, percent body fat (%BF), and resting energy expenditure were determined after 6 and 8 months. Absolute and adiposity-corrected plasma leptin levels were higher in overweight/obese women (37.7 +/- 3.5 ng/mL; 1.01 +/- 0.07 ng.mL-1.%BF-1) than in normal weight women (16.9 +/- 2.2 ng/mL; 0.57 +/- 0.06 ng.mL-1.%BF-1, both P < 0.005 vs. obese), but were not different between the 31%, 23%, and 14% fat diets when body weight was stable. Plasma leptin was highly correlated with BMI (r = 0.81, P < 0.0001), %BF (r = 0.80, P < 0.0001), and fasting plasma insulin (r = 0.61, P < 0.0001). After 8 months on the ad libitum low fat diet, the women had lost an average of 6.9 +/- 1.0% of body mass (-2.0 +/- 0.3 kg/m2, P < 0.0001). In 15 subjects who lost more than 7% of body mass (-12.3 +/- 1.0%), plasma leptin concentrations decreased (-9.6 +/- 1.9 ng/mL, P < 0.0005), and the decrease of plasma leptin per change of adiposity (delta leptin/delta %BF) was greater in overweight/obese women (3.6 +/- 0.5) than in normal weight women (0.9 +/- 0.4, P < 0.01 vs. obese). In 18 other subjects who lost less than 7% of body mass (-2.7 +/- 0.6%), plasma leptin was unchanged (+1.4 +/- 1.4 ng/mL). Overall, the change of plasma leptin was significantly correlated with change of BMI (r = 0.43, P < 0.02), the change of %BF (r = 0.49, P < 0.005), the change of resting energy expenditure (r = 0.40, P < 0.02), and with the change of plasma insulin independently of changes of body adiposity (r = 0.45, P < 0.01). We conclude that plasma leptin concentrations are: 1) not affected by dietary fat content per se; 2) highly correlated with BMI, %BF, and plasma insulin in both overweight/obese and normal weight women; 3) decreased in parallel with plasma insulin after sustained weight loss; and 4) decreased more in overweight/obese than in normal weight women.

Adipose Tissue↗
PubMed1982

[Studies on the measurement of vitamin D derivatives in human plasma. III. Plasma concentrations of vitamin D derivatives in various diseases (author's transl)].

Plasma concentrations of vitamin D3, 25-OH-D3, 24, 25(OH)2D3 and 1, 25(OH)2D3 were measured in patients with various diseases using the multiple assay system previously reported. In patients with hyperparathyroidism, the plasma levels of 1, 25(OH)2D3 tended to increase, while the levels of 24, 25(OH)2D3 tended to decrease in many cases. On the other hand, plasma 1, 25(OH)2D3 levels were low, while 24, 25(OH)2D3 levels were high in patients with hypoparathyroidism. No significant differences in the levels of plasma D3 derivatives among idiopathic-, postoperative- and pseudo- hypoparathyroidism were observed. In a majority of hemodialyzed patients with advanced renal failure who showed no overt bone changes on X-ray films, both the plasma 1, 25(OH)2D3 and 24, 25(OPH)2D3 levels were distributed from normal to very low. In a majority of patients with osteoporosis and hypoparathyroidism, plasma 1, 25(OH)2D3 levels rose quickly after the administration of 1 alpha-OH-D3. In hypophosphatemic vitamin D resistant rickets, however, the response to the relatively large amounts of 1 alpha-OH-D2 was poor, although the concentrations of plasma 24, 25(OH)2D3 were elevated by the 1 alpha-OH-D3 administration in most of these cases. The plasma 1, 25(OH)2D3 and 24, 25(OH)2D3 concentrations in patients with senile osteoporosis were distributed from lower to higher range than those of normal adults. There was a relatively good correlation between plasma levels of 25-OH-D3 and D3 only in cases with plasma D3 levels higher than 5 ng/ml. In addition, a hyperbolic regression curve was obtained between the plasma D3 and 25-OH-D3 ratio. These results may indicate that a possible negative feedback homeostatic mechanism exists between plasma levels of D3 and 25-OH-D3, but only with low plasma levels of D3.

Calcitriol↗
PubMed1979

Interactions among Hageman factor (HG, Factor XII), plasma thromboplastin antecedent (PTA, Factor XI), plasma prekallikrein (PK, Fletcher factor) and high molecular weight kininogen (HMW-K, Fitzgerald factor) in blood coagulation.

Studies of plasmas from individuals with Hageman trait (factor XII deficiency), plasma thromboplastin antecedent (PTA, factor XI) deficiency, Fletcher trait (plasma prekallikrein deficiency) and Fitzgerald trait (high molecular weight-kininogen deficiency) have revealed the importance of these proteins in blood coagulation. The interactions among them, however, are not fully elucidated. We have studied these reactions by two different approaches. (1) In a purified system, high molecular weight kininogen was absolutely required for activation of PTA by HF and ellagic acid (EA). The yield of activated PTA was proportional to the amount of HF, HMW-K, and PTA in the mixtures, suggesting that these three proteins may form a complex in the presence of EA. (2) In experiments with whole plasma, we took advantage of the adsorption of EA to Sephadex gels. When normal plasma or plasma deficient in HF, PK, HMW-K or PTA was exposed to Sephadex-EA and was separated by centrifugation, each supernatant plasma except that deficient in HF shortened the prolonged partial thromboplastin time (PTT) of HF-deficient plasma. Plasma simultaneously depleted of HMW-K, PK and PTA also shortened the PTT of HF-deficient plasma and of plasma depleted of HF and PK, but had virtually no procoagulant effect upon the PTT of plasma depleted of HF and MHW-K. Thus, exposure of HF in plasma to Sephadex-EA appeared to generate a clot-promoting form of HF in the absence of other clotting factors, but its expression required the presence of HMW-K.

Blood Coagulation↗
PubMed1983

Concurrent inductions of avian hepatic lipogenesis, plasma lipids, and plasma apolipoprotein B by estrogen.

The inductions of hepatic fatty acid synthesis, estrogen-specific plasma proteins, plasma lipids, and apolipoproteins by a single subcutaneous injection of diethylstilbestrol (40 mg/kg body weight) have been examined in immature male turkeys. Estrogen induced the appearance of phosvitin, lipovitellin, and apoVLDL-II in the blood plasma. The highest concentrations of these estrogen-specific plasma proteins were observed 48 hr following hormone administration. Estrogen increased the concentration of triglyceride in the liver, predominantly those molecular species containing 16 carbon fatty acids (triglycerides with 53 and 55 carbon atoms). Liver cholesterol was present predominantly as free cholesterol. Although estrogen did not affect the concentrations of free or esterified cholesterol in the liver, the hormone increased the amount of cholesterol esterified with 20-carbon fatty acids and caused a corresponding decrease in cholesterol esterified with 18 carbon fatty acids. Estrogen treatment elevated the plasma triglycerides 55-fold, tripled the plasma phospholipid, and approximately doubled the plasma cholesterol. The de novo synthesis of fatty acids in the liver in vivo was stimulated by estrogen administration, as exhibited by increased 3H2O incorporation into the phospholipids and triglycerides of both liver and plasma. In contrast, hepatic cholesterol synthesis was unaffected. The amounts of newly synthesized triglyceride in the liver and plasma and the specific radioactivities of the plasma triglyceride following 1-hr in vivo labeling periods, 0, 24, 48, and 72 hr after estrogen injection indicate that increased hepatic fatty acid synthesis is a primary and major casuative factor in the development of estrogen-induced hyperglyceridemia in this avian species. The concentration of apolipoprotein B in the plasma increased in parallel with hepatic fatty acid synthesis and the appearance of newly synthesized triglyceride in the plasma, whereas the plasma apolipoprotein A-I level decreased. These observations indicate that in the avian liver estrogen causes a coordination of inductions in the conversion of carbohydrate to triglyceride and in the production of proteins (apolipoprotein B and apoVLDL-II) involved in the assembly of triglyceride-rich lipoprotein particles, leading to hypersecretion of these lipoproteins into the circulation.

Animals↗
PubMed1987

Efficiency of plasma exchange in Guillain-Barré syndrome: role of replacement fluids. French Cooperative Group on Plasma Exchange in Guillain-Barré syndrome.

The goals of this multicenter controlled trial were: (1) to study the short-term effect of plasma exchange in the Guillain-Barré syndrome when applied alone within 17 days of onset of the disease; and (2) to compare two replacement fluids, diluted albumin and fresh frozen plasma (FFP) with regard to efficacy and morbidity. Two hundred twenty patients were included, 111 in the control group, 109 in the plasma exchange group, 57 of whom were assigned to receive albumin and 52 to receive fresh frozen plasma. Treatment consisted of four plasma exchanges of two plasma volumes each, initiated on the day of randomization and repeated on alternate days. Significant short-term benefits appeared in the group that received plasma exchange as demonstrated by the reduction in the proportion of patients who required assisted ventilation after randomization, and the decrease in time before beginning weaning from ventilator, time to onset of motor recovery, and time to walk with and without assistance. No statistically significant difference was found between the group that received albumin and the group that received fresh frozen plasma. Incidents during exchanges and complications related to the plasma exchange were more frequent in patients who received fresh frozen plasma. Plasma exchange is beneficial in Guillain-Barré syndrome when it is carried out early in the course of the disease. Given its risks and the lack of its clear superiority over albumin, however, we recommend that fresh frozen plasma be abandoned in the treatment of Guillain-Barré syndrome.

Adult↗
PubMed1993

Coagulation parameters of CPD fresh-frozen plasma and CPD cryoprecipitate-poor plasma after storage at 4 degrees C for 28 days.

A pilot study was performed on the storage of plasma and cryosupernatant plasma at 4 degrees C for up to 28 days. Eight bags, four of CPD fresh-frozen plasma (FFP) and four of CPD cryosupernatant plasma (CSP, plasma without cryoprecipitate), were sampled during storage for assays of pH; factors V, VIII, IX, and XI; fibrinogen; prothrombin time; activated partial thromboplastin time (APTT); plasma protein electrophoresis; viscosity; and C1q binding. No changes were found in viscosity or the plasma protein electrophoretic pattern, and there was no detectable immune complex formation. The fibrinogen concentration remained constant, and the prothrombin time showed a gradual increase of 2.5 seconds for both groups of plasma. The labile coagulation factor V decreased gradually for FFP and CSP to 58 and 64 percent of its initial value, respectively (51 +/- 8% and 54 +/- 6% of the value of fresh pooled plasma). Factor VIII decreased to 36 percent of its initial value in FFP (48 +/- 14% of fresh pooled plasma). In CSP, factor VIII decreased after 28 days to 7 percent of its initial value (7 +/- 1% of fresh pooled plasma). The APTT increased for FFP from 28 to 35.8 +/- 1.1 seconds and for CSP from 36 to 49.5 +/- 4.9 seconds. The only chemical change observed for both plasmas was a rise in pH, from 7.27 to 7.56, after 28 days. The results of this pilot study indicate that FFP can be stored at 4 degrees C for 28 days with sufficient recovery of coagulation factors to maintain hemostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Factors↗