Biological Activity of Low-Molecular Weight Dextran 40. The Effect on Serum Proteins, Plasma Blood Clotting Factors and Erythrocyte Sedimentation Rate

1973 ◽  
Vol 1 (3) ◽  
pp. 194-203
Author(s):  
Witold Rudowski ◽  
Ewa Kostrzewska ◽  
Anita Gregor ◽  
Angela Naleçzyńska

Dextran 40 infused in doses from 1.2 to 1.5 g/kg body weight decreases the concentration of proteins in the plasma and reduces the total amount of circulating protein. Dextran 40 in vitro precipitates high-molecular weight proteins participating in blood clotting, such as factor VIII and fibrinogen and, if infused, decreases their plasma levels. Addition in vitro of Dextran 40 to blood with a high ESR reduces the value proportionally to the concentration of dextran in the blood sample: after infusion of Dextran 40 the ESR decreases by a mean value of 19.9% after infusion of 500 ml and by 36.2% after 1000 ml. No bleeding was noted with these infusions.

1971 ◽  
Vol 17 (11) ◽  
pp. 1109-1113 ◽  
Author(s):  
R C Robbins ◽  
R H Hammer ◽  
C F Simpson

Abstract Methoxylated flavonoids containing one or three to seven methoxyl groups were compared for inhibitory activity on erythrocyte aggregation in vitro. A serial erythrocyte sedimentation procedure was used, in which the compounds are incubated in blood maintained in thermal and flow equilibria. All compounds tested (30 µmol/liter) significantly inhibited erythrocyte aggregation: hesperidin < tri-O-methylapigenin < tetra-O-methylscutellarein < tangeretin < heptamethoxyflavone < nobiletin < sinensetin. The most active compound, sinensetin, contained methoxyl groups at the 3',4',5,6,7 positions. Compounds with fewer methoxyl groups were significantly less active (P < 0.01), as were compounds with additional methoxyl groups at the 3 and 8 positions. On a molar basis, compounds containing five to seven methoxyl groups were several fold more active on erythrocyte aggregation than was low-molecular-weight dextran.


2002 ◽  
Vol 734 ◽  
Author(s):  
Tomohiko Yoshioka ◽  
Kanji Tsuru ◽  
Satoshi Hayakawa ◽  
Akiyoshi Osaka

ABSTRACTγ-Aminopropyltriethoxysilane (γ-APS) was grafted on stainless-steel and titanium substrates, and subsequently alginic acid layer was immobilized on them. Their surfaces were characterized with X-ray photoelectron spectroscopy (XPS) and contact angle measurement. Blood compatibility of thus obtained substrates was evaluated in terms of both the number of the adhered platelets and blood clotting factors for plasma contacted with the substrates such as active partial thromboplastin time (PTT), prothrombin time (PT), and amount of fibrinogen (Fib). The steel and titanium substrates with alginic acid layer did not affect blood clotting factors. In vitro platelet adhesion assay indicated that those substrates adhered less number of platelets than non-treated substrates. Hence the alginic acid immobilization leads to blood compatible surfaces.


1982 ◽  
Vol 48 (02) ◽  
pp. 120-124 ◽  
Author(s):  
J-M Freyssinet ◽  
D Thevenon ◽  
A Souque ◽  
M Suscillon

SummaryWheat germ agglutinin (WGA) and concanavalin A (Con-A) (also red kidney bean agglutinin, PHA) have been found to be inhibitors of plasma clotting in vitro. At 40 µg/ml and 250 µg/ml (4.4 µM and 10 µM in carbohydrate binding sites, final concentrations) respectively, WGA and Con-A are able to double the activated partial thromboplastin time of normal human control plasma. Their inhibitory effect is due to their capacity to interact with the carbohydrate portion of blood clotting factors. It is totally abolished in the presence of specific saccharides for WGA or Con-A and is attenuated in the presence of 4% (v/v, final concentration) of human erythrocytes. The action of WGA is mediated by its ability to interact with N-acetylneuraminic acid. When purified phospholipid vesicles plus kaolin are used as an activator instead of cephalidin, this effect persists to the same extent. These two lectins also prolong the plasma clotting time using Russell's viper venom plus purified phospholipid vesicles as an activator. Quick's time was also prolonged by WGA and Con-A but to a lesser extent in this case. WGA can interact directly with some purified blood clotting factors (IX, X and II) in a classical lectin-glycoprotein precipitin reaction. When assessed at individual factors level in whole plasma using clotting assays, direct inhibitions by WGA are only apparent.


1971 ◽  
Vol 17 (5) ◽  
pp. 433-437 ◽  
Author(s):  
R C Robbins

Abstract Flavonoids were investigated for activity on blood cell aggregation. A procedure for measuring serial erythrocyte sedimentation rate (ESR) was used to test the effect of five flavonoids (hesperidin, quercetin, rutin, tangeretin, and naringin) on aggregation in vitro. The activity of the flavonoids was compared with that of quinine and low molecular weight dextran (LMD), both of which demonstrably decrease blood cell aggregation in vivo and in vitro. At a blood concentration of 50 µmol/liter the flavonoids, quinine, and LMD all showed significant effects (P < 0.05) on aggregation, the order of retardation of ESR being rutin < quercetin < LMD < hesperidin < quinine < tangeretin. Naringin-treated blood had a higher ESR than control blood. The effect of flavonoids on blood cell aggregation suggests how they may act against increased capillary permeability and fragility, reduce symptoms in disease, and protect against effects of various traumas and stresess.


1994 ◽  
Vol 72 (06) ◽  
pp. 942-946 ◽  
Author(s):  
Raffaele Landolfi ◽  
Erica De Candia ◽  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Armando Antinori ◽  
...  

SummarySeveral “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.


1961 ◽  
Vol 06 (01) ◽  
pp. 015-024 ◽  
Author(s):  
Sven Erik Bergentz ◽  
Oddvar Eiken ◽  
Inga Marie Nilsson

Summary1. Infusions of low molecular weight dextran (Mw = 42 000) to dogs in doses of 1—1.5 g per kg body weight did not produce any significant changes in the coagulation mechanism.2. Infusions of high molecular weight dextran (Mw = 1 000 000) to dogs in doses of 1—1.5 g per kg body weight produced severe defects in the coagulation mechanism, namely prolongation of bleeding time and coagulation time, thrombocytopenia, pathological prothrombin consumption, decrease of fibrinogen, prothrombin and factor VII, factor V and AHG.3. Heparin treatment of the dogs was found to prevent the decrease of fibrinogen, prothrombin and factor VII, and factor V otherwise occurring after injection of high molecular weight dextran. Thrombocytopenia was not prevented.4. In in vitro experiments an interaction between fibrinogen and dextran of high and low molecular weight was found to take place in systems comprising pure fibrinogen. No such interaction occurred in the presence of plasma.5. It is concluded that the coagulation defects induced by infusions of high molecular weight dextran are due to intravascular coagulation.


1967 ◽  
Vol 18 (03/04) ◽  
pp. 634-646 ◽  
Author(s):  
N Thurnherr

SummaryBlood clotting investigations have been executed in 25 patients who have undergone open heart surgery with extracorporeal circulation. A description of alterations in the activity of blood clotting factors, the fibrinolytic system, prothrombin consumption and platelets during several phases of the operation is given.


1986 ◽  
Vol 56 (03) ◽  
pp. 318-322 ◽  
Author(s):  
V Diness ◽  
P B Østergaard

SummaryThe neutralization of a low molecular weight heparin (LHN-1) and conventional heparin (CH) by protamine sulfate has been studied in vitro and in vivo. In vitro, the APTT activity of CH was completely neutralized in parallel with the anti-Xa activity. The APTT activity of LHN-1 was almost completely neutralized in a way similar to the APTT activity of CH, whereas the anti-Xa activity of LHN-1 was only partially neutralized.In vivo, CH 3 mg/kg and LHN-1 7.2 mg/kg was given intravenously in rats. The APTT and anti-Xa activities, after neutralization by protamine sulfate in vivo, were similar to the results in vitro. In CH treated rats no haemorrhagic effect in the rat tail bleeding test and no antithrombotic effect in the rat stasis model was found at a protamine sulfate to heparin ratio of about 1, which neutralized APTT and anti-Xa activities. In LHN-1 treated rats the haemorrhagic effect was neutralized when APTT was close to normal whereas higher doses of protamine sulfate were required for neutralization of the antithrombotic effect. This probably reflects the fact that in most experimental models higher doses of heparin are needed to induce bleeding than to prevent thrombus formation. Our results demonstrate that even if complete neutralization of APTT and anti-Xa activities were not seen in LHN-1 treated rats, the in vivo effects of LHN-1 could be neutralized as efficiently as those of conventional heparin. The large fall in blood pressure caused by high doses of protamine sulfate alone was prevented by the prior injection of LHN-1.


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