scholarly journals In vitro relationship between the blood nafamostat concentration and activated coagulation time

2003 ◽  
Vol 50 (6) ◽  
pp. 621-622
Author(s):  
Hiroshi Iwama ◽  
Kazuhiro Watanabe ◽  
Shinju Obara
1991 ◽  
Vol 66 (02) ◽  
pp. 213-217 ◽  
Author(s):  
Arthur P Bode ◽  
William J Castellani ◽  
Edna D Hodges ◽  
Susan Yelverton

SummaryThe effect of lysed platelets on the activated coagulation time (ACT) was studied in heparinized whole blood during titration with protamine. Frozen-thawed washed platelet suspension, or a chromatography fraction thereof, or autologous frozen-thawed platelet-rich plasma was added in various dilutions to freshly drawn blood anticoagulated with 3,000 USP units/1 heparin. After a 10 min incubation, the amount of protamine needed to restore the ACT to baseline ("protamine titration dose") was determined. We found that the protamine titration dose decreased in proportion to the amount of lysed platelet material added; expressed as a percentage of the total number of platelets present, each unit increase in lysed platelets produced a 1.7% ±0.8 (SD) reduction in the protamine dose needed to normalize the ACT. A heparin activity assay showed that this effect was not due to antiheparin activity of lysed platelets such as platelet factor 4 (PF4). Our data indicate that the procoagulant activity of platelet membranes reduced the sensitivity of the ACT to heparin. These findings suggest that membranous platelet microparticles may cause an inaccurate calculation, based on the ACT, of a protamine dose to reverse heparin anticoagulation in cardiopulmonary bypass procedures.


2000 ◽  
Vol 90 (5) ◽  
pp. 1076-1079 ◽  
Author(s):  
Jerrold H. Levy ◽  
Felix Montes ◽  
Fania Szlam ◽  
Christopher D. Hillyer

1979 ◽  
Author(s):  
I. Fabian ◽  
M. Aronson

Heparin rebound is occasionally encountered following protamin sulfate administration for the neutralization of excess of heparin. in these situations the anticoagulatory properties of heparin are initially abolished, but within several hours the blood display again an increased clotting time. The purpose of this work was to try to reproduce the phenomenon under in vitro conditions, and to provide a working hypothesis for its explanation. Under the condition used the following parameters were obtained (according to the APTT method): clotting time of untreated plasma 50-55 seconds; with the addition of 4 units heparin/ml plasma>3 minutes; and with the addition of 50-100 μg of protamin to the heparinized plasma the clotting time reverts to 50-55 seconds. It was, however, found that incubation of heparin-protamin complex with the plasma at 37° for several hours, reduced the effectivity of the protamin, in other words, a longer coagulation time was observed. Subsequently, we found by electrophoretical methods that (heparin bound) protamin is proteolitically degraded upon incubation in plasma, the anticoagulatory properties of the heparin remaining intact. in summary, our results are compatible with the hypothesis that heparin rebound can be explained by the degradation of protamin by plasma enzymes and the release of this newly available heparin Into the circulation. The importance of this phenomenon in conjunction with other observations previously described by us are discussed.


1991 ◽  
Vol 26 (12) ◽  
pp. 1141
Author(s):  
D. S Sallee ◽  
C. J Becker ◽  
O Bouds ◽  
J Benenati ◽  
C Zemel ◽  
...  

2020 ◽  
Vol 34 (9) ◽  
pp. 2369-2374
Author(s):  
Antoine G. Rochon ◽  
Sylvain Bélisle ◽  
Pierre Couture ◽  
Annik Fortier ◽  
Jean-Sébastien Lebon ◽  
...  

Blood ◽  
1952 ◽  
Vol 7 (7) ◽  
pp. 710-720 ◽  
Author(s):  
S. VAN CREVELD ◽  
M. M. P. PAULSSEN

Abstract Transfusions of heparinized plasma have a greater and more lasting effect on the coagulation time of hemophiliacs than transfusions of citrated plasma. Both in vitro and in vivo, heparinized plasma causes in hemophiliacs a far greater consumption of prothrombin as determined with the two-stage method than citrated plasma. In using the one-stage method no important differences in prothrombin activity are found after transfusions of heparinized and of citrated plasma respectively. This fact was thought to be connected with the more or less rapid appearance of an accelerator. Its a hemophiliac with a circulating anticoagulant, transfusions of heparinized plasma were unable to shorten the coagulation time to any important degree, nor did these transfusions cause an important decrease of serum prothrombin as determined by the two-stage method.


1979 ◽  
Author(s):  
I. Fabian ◽  
M. Aronson

Heparin rebound is occasionally encountered following protamin sulfate administration for the neutralization of excess of heparin. In these situations the anticoagulatory properties of heparin are initially abolished, but within several hours the blood display again an increased clotting time. The purpose of this work was to try to reproduce the phenomenon under in vitro conditions, and to provide a working hypothesis for its explanation. Under the condition used the following parameters were obtained (according to the APTT method): clotting time of untreated plasma 50-55 seconds; with the addition of 4 units heparin/ml plasma>3 minutes; and with the addition of 50-100 μg of protamin to the heparinized plasma the clotting time reverts to 50-55 seconds. It was, however, found that incubation of heparin-protamin complex with the plasma at 37° for several hours, reduced the effectivity of the Protamin, in other words, a longer coagulation time was observed. Subsequently, we found by electrophoretical methods that (heparin bound) protamin is proteolitically degraded upon incubation in plasma, the anticoagulatory properties of the heparin remaining intact. In summary, our results are compatible with the hypothesis that heparin rebound can be explained by the degradation of Protamin by plasma enzymes and the release of this newly available heparin in to the circulation. The importance of this phenomenon in conjunction with other observations previously described by us are discussed.


Molecules ◽  
2020 ◽  
Vol 25 (1) ◽  
pp. 177 ◽  
Author(s):  
Changqin Li ◽  
Miyun Hu ◽  
Shengjun Jiang ◽  
Zhenhua Liang ◽  
Jinmei Wang ◽  
...  

Astragalin, isolated from flowers of Rosa chinensis Jacq., is a kind of flavonoid, with anti-inflammatory, antioxidant, antiviral, analgesic, antibacterial, antiallergic, and antihepatotoxic effects. However, no studieson the procoagulant effect of astragalin have been reported. This study aimed to investigate the procoagulant activity of astragalin and its mechanism. Its procoagulant effect was investigated by activated partial thromboplastin time (APTT), thrombin time (TT), prothrombin time (PT), and fibrinogen (FIB) in vitro, and a rat model established by heparin sodium was used to evaluate the mechanism for the procoagulant effect in vivo. The results showed that astragalin had good procoagulant effects compared with the control group in vitro. Compared with the model group in vivo, astragalin could shorten the coagulation time and significantly increase the number of platelets. Meanwhile, astragalin could significantly reduce the effectual time of PT and APTT and increase the content of FIB. The contents of 6-keto-PGF1α and eNOS significantly decreased. Astragalin could increase whole blood viscosity (WBV), plasma viscosity (PV), erythrocyte sedimentation rate (ESR) and packedcell volume (PCV). All of the above revealed that astragalin had good procoagulant effects by promoting the intrinsic and extrinsic coagulation system.


Sign in / Sign up

Export Citation Format

Share Document