scholarly journals A comparison of the in vitro effects of three fibrinogen concentrates on clot strength in blood samples from cardiac surgery patients

Author(s):  
Henrik Stolt ◽  
Caroline Shams Hakimi ◽  
Sukhi Singh ◽  
Anders Jeppsson ◽  
Martin Karlsson

1992 ◽  
Vol 72 (4) ◽  
pp. 1291-1296 ◽  
Author(s):  
O. B. Nielsen ◽  
G. Lykkeboe

Plasma and erythrocyte K+ were monitored during storage and tonometry of blood samples taken from resting rainbow trout, Oncorhynchus mykiss. During storage of arterial blood samples, plasma K+ concentration increased by 38% in 12 min. During extended tonometry of blood with a pH near 7.9 and full hemoglobin-bound oxygen (HbO2) saturation the erythrocytes showed a net loss of K+. Plasma K+ concentration increased from 2.9 mM to a near steady-state value of 5.6 mM. When tonometered at a pH near 7.2 and a HbO2 saturation at approximately 4% the erythrocytes took up K+, leading to a dramatic reduction in plasma K+ concentration to 0.2 mM. This net uptake was stimulated by isoprenaline and was inhibited by ouabain. It is concluded that net erythrocyte K+ uptake and loss can be induced in trout by changes in blood pH or HbO2 saturation in vitro.



1987 ◽  
Author(s):  
E Seifried ◽  
P Tanswell

Monitoring of systemic effects during rt-PA therapy has shown of depletion of fibrinogen-antiplasmin, plasminogen and other hemostatic factors. Because in vitro activation of plasminogen may occur between blood collection and freezing and thawing before assaying we analysed the influence of 0,0.2, 2.0 and 10.0,ug rt-PA/ml citrate blood (final conc.) on hemostatic and fibrinolytic parameters and its inhibition by 3 different inhibitors. Addition of rt-PA to citrated whole blood without an inhibitor induced a concentration-dependent depletion of Fbg, Plgα2-Apl,α2-M, C1 - I, α2-Atrp, a loss of activity of FV, VIII,IX, XIII and alterations of the global coagulation assays. No effect of rt-PA was observed on F II, VII, X, XI, XII, AT III and Protein C. To prevent in vitro fibrinogenolysis 0.1, 0.5 and 1 mg/ml of a polyclonal sheep anti-rt-PA-antibody, 0.3, 1.0 and 10 Aimol/1 PPACK (D-Phe-Pro-Arg-CH2Cl), 75 and 150 KlU/ml aprotinin (final conc.) and saline as a control were added to pooled citrate blood.All samples containing rt-PA and/or inhibitors and/or saline were incubated for 45 min on ice, centrifuged, aliquotted, snap frozen and stored at ™20° C until analysis. Pretreatment of blood samples with anti-rt-PA IgG prevented interferences with all fibrinolytic and most clotting assays in plasma at a dose of 2 ,ug rt-PA/ ml. PPACK was of limited utility in clotting assays, but enabled correct analysis of fibrinolytic assays. Aprotinin was suitable only for a restricted range of both assay types. It is concluded that collection of blood samples on an appropriate antibody may be the most suitable procedure to get correct measurements of in-vivo effects of rt-PA on the hemostatic system in patients undergoing fibrinolytic therapy.



2013 ◽  
Vol 74 (4) ◽  
pp. 567-571 ◽  
Author(s):  
Laura R. Tonkin ◽  
Nolie K. Parnell ◽  
Daniel F. Hogan




2015 ◽  
Vol 5 (1) ◽  
pp. 5-10
Author(s):  
Maida Rakanovic-Todic ◽  
Slavka Ibrulj ◽  
Lejla Burnazovic-Ristic ◽  
Amra Catovic ◽  
Izeta Aganovic-Musinovic ◽  
...  

Introduction: The met-enkephalin (1-5 Adrenorphin) and tridecactide (alpha-corticotropin 1-13) combination is used in the multiple sclerosis (MS) immuno-modulatory treatment. A testing of cytogenetic effects of met-enkephalin resulted in reductions of lymphocytic aberrations in the in the lymphocytes of the peripheral blood (PBL) of patients with immune-mediated diseases. The aim of this research is to evaluate the in vitro effects of the combination of the met-enkephalin and tridecactide on the number and the type of chromosome aberrations in PBL of the MS patients. Methods: We used blood samples from seven female patients with the diagnosis multiple sclerosis based on a McDonald Diagnostic Criteria. The tested combination, met-enkephalin and alpha-ACTH 1-13 was added at three different concentrations and constant volume. Results: Results showed that the combination of tested substances did not reduce the number of structural aberrations, although the treatment did not result in severe aberrations such as ring, fragmented, and dicentric chromosomes. Furthermore, it elicited an increase in the number of numerical aberrations and aneuploidy after the treatment with the test combo. Conclusion: As the changes in ploidy significantly change the DNA as well as the biochemical cell phenotype, we concluded that more research in this field should be conducted, including both toxicological as well as the pharmacodynamic considerations.



1997 ◽  
Vol 85 (6) ◽  
pp. 519-522 ◽  
Author(s):  
Elbio A D'Amico ◽  
Dalton A.F Chamone ◽  
Sérgio P Bydlowski


Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  


1990 ◽  
Vol 64 (03) ◽  
pp. 402-406 ◽  
Author(s):  
M D Oethinger ◽  
E Seifried

SummaryThe present in vitro study investigated dose-, time- and temperature-dependent effects of two-chain urokinase plasminogen activato(u-PA, urokinase) on normal citrated plasma. When 10 μg/ml u-PA wereadded to pooled normal plasma and incubated for 30 min at an ambient temperature (25° C), α2-antiplas-min decreased to 8% of the control value. Incubation on ice yielded a decrease to 45% of control,whereas α2-antiplasmin was fully consumed at 37° C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25° C. Thrombin time prolonged to 190% of control.Various inhibitors were studied with respect to their suitability and efficacy to prevent these in vitro effects. Aprotinin exhibited a good protective effect on fibrinogen at concentrations exceeding 500 KlU/ml plasma. Its use, however, was limited due to interferences with some haemostatic assays. We could demonstrate that L-Glutamyl-L-Glycyl-L-Arginyl chloromethyl ketone (GGACK) and a specific polyclonal anti-u-PA-antibody (anti-u-PA-IgG) effectively inhibited urokinase-induced plasmin generation without interfering with haemostatic assays. The anti-u-PA-antibody afforded full protection ofα2-antiplasmin at therapeutic levels of u-PA.It is concluded that u-PA in plasma samples from patients during thrombolytic therapy may induce in vitro effects which should be prevented by the use of a suitable inhibitor such as GGACK or specific anti-u-PA-antibody.



1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.



1987 ◽  
Vol 58 (03) ◽  
pp. 921-926 ◽  
Author(s):  
E Seifried ◽  
P Tanswell

SummaryIn vitro, concentration-dependent effects of rt-PA on a range of coagulation and fibrinolytic assays in thawed plasma samples were investigated. In absence of a fibrinolytic inhibitor, 2 μg rt-PA/ml blood (3.4 μg/ml plasma) caused prolongation of clotting time assays and decreases of plasminogen (to 44% of the control value), fibrinogen (to 27%), α2-antiplasmin (to 5%), FV (to 67%), FVIII (to 41%) and FXIII (to 16%).Of three inhibitors tested, a specific polyclonal anti-rt-PA antibody prevented interferences in all fibrinolytic and most clotting assays. D-Phe-Pro-Arg-CH2Cl (PPACK) enabled correct assays of fibrinogen and fibrinolytic parameters but interfered with coagulometric assays dependent on endogenous thrombin generation. Aprotinin was suitable only for a restricted range of both assay types.Most in vitro effects were observed only with rt-PA plasma concentrations in excess of therapeutic values. Nevertheless it is concluded that for clinical application, collection of blood samples on either specific antibody or PPACK is essential for a correct assessment of in vivo effects of rt-PA on the haemostatic system in patients undergoing fibrinolytic therapy.



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