Activity of Synthetic Phospholipids in Blood Coagulation

1965 ◽  
Vol 13 (01) ◽  
pp. 194-217 ◽  
Author(s):  
F. J. M Daemen ◽  
C van Arkel ◽  
H Ch. Hart ◽  
C van der Drift ◽  
L. L. M van Deenen
Keyword(s):  
Blood Coagulation ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Serine ◽  
Maximum Activity ◽  
Fatty Acid Constituent ◽  
Coagulant Activity ◽  
Negative Surface ◽  
High Concentrations ◽  
Poly Unsaturated Fatty Acid

Summary1. An investigation was made into the activity of synthetic phospholipids on blood coagulation in vitro, utilizing synthetic substances including phosphatidyl ethanolamine and phosphatidyl serine containing a poly-unsaturated fatty acid constituent.2. Applying a one-stage recalcification test, phosphatidyl serine was found to act at high concentrations as anticoagulant. No clot-promoting activity was observed after addition of individual phospholipids. However, several combinations of phospholipids, e.g. phosphatidyl ethanolamine with phosphatidyl serine or certain mixtures of lecithin with phosphatidylserine, shortened the clotting time.3. In the thromboplastin generation test phosphatidyl ethanolamine exhibited some acceleratory activity without being able, however, to replace crude brain cephalin completely. However, optimal coagulant activity was produced by mixtures of synthetic phospholipids viz, phosphatidyl ethanolamine with phosphatidyl serine, phosphatidic acid or (isolated) cardiolipin and by certain combinations of lecithin and phosphatidyl serine.4. In both assay systems the maximum activity of each phospholipid combination was found to be related within certain limits to the ratio of both compounds. It is concluded that the coagulant activity of phospholipids in vitro is not to be attributed to a certain type of phospholipid or a defined mixture. The results obtained with the synthetic compounds appear to support the view that a particular negative surface charge of the phospholipid micelles is a prerequisite for maximal clot-promoting activity of phospholipids.

METABOLISM OF EHRLICH ASCITES TUMOR IN VITRO: SUBCELLULAR DISTRIBUTION OF PHOSPHOLIPIDS NEWLY FORMED FROM14C-LABELED PRECURSORS

1966 ◽  
Vol 44 (11) ◽  
pp. 1461-1468 ◽  
Author(s):  
V. Donisch ◽  
R. J. Rossiter
Keyword(s):  
Microsomal Fraction ◽  
Phosphatidyl Ethanolamine ◽  
Lipid Fraction ◽  
Specific Radioactivity ◽  
Phosphatidyl Inositol ◽  
Phosphatidyl Serine ◽  
Ethanolamine Phosphatidyl ◽  
Ehrlich Ascites ◽  
Ethanolamine Plasmalogen

When Ehrlich ascites cells were incubated in a suitable medium containing choline-1,2-14C, ethanolamine-1,2-14C, L-serine-14C, or glycerol-1-14C, radioactivity was recovered from the lipid fraction. With choline-1,2-14C, radioactivity was incorporated into the three choline-containing phospholipids, lecithin, choline plasmalogen, and sphingomyelin. Radioactivity from ethanolamine-1,2-14C was incorporated into phosphatidyl ethanolamine, ethanolamine plasmalogen, choline plasmalogen, and lecithin. Radioactivity from L-serine-14C was incorporated into phosphatidyl serine, serine plasmalogen, and phosphatide acid, with lesser amounts into phosphatidyl ethanolamine, lecithin, ethanolamine plasmalogen, choline plasmalogen, and sphingomyelin. Radioactivity from glycerol-1-14C was incorporated into the glycerophosphatides, phosphatidic acid, lecithin, phosphatidyl ethanolamine, phosphatidyl serine, phosphatidyl inositol, and choline plasmalogen. Radioactivity from this precursor was also incorporated into sphingomyelin.In all instances, radioactivity was recovered from the phosphatides in the nuclear, mitochondrial, and microsomal fractions of the tumor. Usually, the specific radioactivity of the phosphatides in the microsomal fraction exceeded that in the other two subcellular fractions.

BIOSYNTHESIS OF LECITHIN IN. BRAIN AND DEGENERATING NERVE. PARTICIPATION OF CYTIDINE DIPHOSPHATE CHOLINE

1957 ◽  
Vol 35 (1) ◽  
pp. 945-951 ◽  
Author(s):  
R. J. Rossiter ◽  
I. M. McLeod ◽  
K. P. Strickland
Keyword(s):  
Sciatic Nerve ◽  
Metabolic Pathways ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Serine ◽  
Two Dimensional ◽  
Naturally Occurring ◽  
Hydrolysis Products ◽  
Cytidine Diphosphate

The radioactivity of cytidine diphosphate choline labelled with P32(CMP-P32Ch) was incorporated in vitro into the phosphatides of both hypotonic homogenates of rat brain and mitochondria prepared from isotonic sucrose homogenates. With both preparations the incorporation was increased by addition of D-α,β-diglycerides prepared enzymatically from naturally-occurring lecithins.Hydrolysis of the labelled phosphatides, followed by separation of the hydrolysis products by two-dimensional paper chromatography, indicated that most of the radioactivity was in lecithin (phosphatidyl choline). Only traces of activity were present in phosphatidyl ethanolamine and phosphatidyl serine. There was also some radioactivity in an alkali-stable fraction that was designated 'sphingomyelin'.These findings are consistent with the view that the phosphatides of brain are formed in situ from smaller molecules and that the metabolic pathways for their formation are similar to those postulated by Kennedy and colleagues for the biosynthesis of phosphatides in chicken liver.The radioactivity of CMP-P32Ch also was incorporated into the phosphatides of homogenates of rat sciatic nerve. This incorporation was greater in homogenates prepared from nerves removed 13 days after previous section. It is suggested that these and other increases, found in the in vitro labelling of phosphatides in nerves degenerating after previous section, reported elsewhere, represent an increase in the potentiality of the nerve for remyelination. These increases are associated with the increase in the number of Schwann cells in the nerve.

scholarly journals Contradictory functions of sulfatide in the blood coagulation system as coagulant and anticoagulant.

1998 ◽  
Vol 45 (2) ◽  
pp. 493-499 ◽  
Author(s):  
M Kyogashima ◽  
J Onaya ◽  
A Hara ◽  
T Taketomi
Keyword(s):  
Blood Coagulation ◽  
Thrombus Formation ◽  
Coagulation Factor ◽  
Coagulation System ◽  
Factor Xii ◽  
Blood Coagulation System ◽  
Coagulant Activity ◽  
J 13

Sulfatide (galactosylceramide I3 -sulfate) has been reported to activate blood coagulation factor XII (Hageman factor), which suggests that it exhibits coagulant activity (Fujikama et al., 1980 Biochemistry 19, 1322-1330) However, sulfatide administered into animals as a bolus shot without subsequent thrombus formation, prolonged conventional clotting times and bleeding time (Hara et al., 1996 Glycoconjugate J. 13, 187-194). These findings suggest that it may exhibit anticoagulant rather than coagulant activity. Following this suggestion we found in vitro that binding of sulfatide to fibrinogen resulted in disturbance of fibrin formation. To examine a possible pharmacological effect of sulfatide on blood coagulation in vivo we continuously infused sulfatide into rats through plastic cannulae and found formation of giant thrombi around the tips of the cannulae. These data suggest that sulfatide may exhibit contradictory functions in the blood coagulation system.

scholarly journals Sickled erythrocytes accelerate clotting in vitro: an effect of abnormal membrane lipid asymmetry

Blood ◽  
1981 ◽  
Vol 58 (2) ◽  
pp. 398-401 ◽  
Author(s):  
D Chiu ◽  
B Lubin ◽  
B Roelofsen ◽  
LL van Deenen
Keyword(s):  
Phosphatidyl Ethanolamine ◽  
Phospholipid Composition ◽  
Coagulation Factors ◽  
Phosphatidyl Serine ◽  
Membrane Lipid ◽  
Clotting Time ◽  
Blood Coagulation Factors ◽  
Intact Cells ◽  
Lipid Asymmetry

Abstract A membrane lipid abnormality induced by sickling and found as a permanent alteration in the irreversibly sickled cell (ISC) is the rearrangement of phosphatidyl ethanolamine (PE) and phosphatidyl serine (PS) from the inner to the exterior side of the lipid bilayer. Since PS can provide a catalytic surface for the binding of blood coagulation factors and thus can exhibit procoagulant activity, we investigated the influence of oxy and deoxy reversibly sickled cells (RSC) ass well as ISC on clotting in vitro. Red blood cells (RBC), as the source of phospholipid, were added to platelet-poor citrated plasma containing Russell's viper venom (RVV) and clotting time was measured after recalcification. The clotting time after addition of normal RBC and oxy- RSC was similar to the saline blank (100 sec). In contrast, both oxy- ISC and deoxy completely sickled RSC shortened clotting time by 30%. Using liposomes prepared with identical phospholipid composition to the outer lipid leaflet of either normal RBC, RSC or ISC clotting times similar to those with intact cells were achieved. Since the liposomes did not contain protein, accentuation of clotting appears to be related to abnormal phospholipid organization, in particular to the abnormal exposure to aminophospholipids on the outer surface of the membrane. This abnormality may contribute to the pathogenesis of the vaso- occlusive episode in sickle cell anemia.

scholarly journals Sickled erythrocytes accelerate clotting in vitro: an effect of abnormal membrane lipid asymmetry

Blood ◽  
1981 ◽  
Vol 58 (2) ◽  
pp. 398-401 ◽  
Author(s):  
D Chiu ◽  
B Lubin ◽  
B Roelofsen ◽  
LL van Deenen
Keyword(s):  
Phosphatidyl Ethanolamine ◽  
Phospholipid Composition ◽  
Coagulation Factors ◽  
Phosphatidyl Serine ◽  
Membrane Lipid ◽  
Clotting Time ◽  
Blood Coagulation Factors ◽  
Intact Cells ◽  
Lipid Asymmetry

A membrane lipid abnormality induced by sickling and found as a permanent alteration in the irreversibly sickled cell (ISC) is the rearrangement of phosphatidyl ethanolamine (PE) and phosphatidyl serine (PS) from the inner to the exterior side of the lipid bilayer. Since PS can provide a catalytic surface for the binding of blood coagulation factors and thus can exhibit procoagulant activity, we investigated the influence of oxy and deoxy reversibly sickled cells (RSC) ass well as ISC on clotting in vitro. Red blood cells (RBC), as the source of phospholipid, were added to platelet-poor citrated plasma containing Russell's viper venom (RVV) and clotting time was measured after recalcification. The clotting time after addition of normal RBC and oxy- RSC was similar to the saline blank (100 sec). In contrast, both oxy- ISC and deoxy completely sickled RSC shortened clotting time by 30%. Using liposomes prepared with identical phospholipid composition to the outer lipid leaflet of either normal RBC, RSC or ISC clotting times similar to those with intact cells were achieved. Since the liposomes did not contain protein, accentuation of clotting appears to be related to abnormal phospholipid organization, in particular to the abnormal exposure to aminophospholipids on the outer surface of the membrane. This abnormality may contribute to the pathogenesis of the vaso- occlusive episode in sickle cell anemia.

BIOSYNTHESIS OF LECITHIN IN. BRAIN AND DEGENERATING NERVE. PARTICIPATION OF CYTIDINE DIPHOSPHATE CHOLINE

1957 ◽  
Vol 35 (11) ◽  
pp. 945-951 ◽  
Author(s):  
R. J. Rossiter ◽  
I. M. McLeod ◽  
K. P. Strickland
Keyword(s):  
Sciatic Nerve ◽  
Metabolic Pathways ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Serine ◽  
Two Dimensional ◽  
Naturally Occurring ◽  
Hydrolysis Products ◽  
Cytidine Diphosphate

The radioactivity of cytidine diphosphate choline labelled with P32(CMP-P32Ch) was incorporated in vitro into the phosphatides of both hypotonic homogenates of rat brain and mitochondria prepared from isotonic sucrose homogenates. With both preparations the incorporation was increased by addition of D-α,β-diglycerides prepared enzymatically from naturally-occurring lecithins.Hydrolysis of the labelled phosphatides, followed by separation of the hydrolysis products by two-dimensional paper chromatography, indicated that most of the radioactivity was in lecithin (phosphatidyl choline). Only traces of activity were present in phosphatidyl ethanolamine and phosphatidyl serine. There was also some radioactivity in an alkali-stable fraction that was designated 'sphingomyelin'.These findings are consistent with the view that the phosphatides of brain are formed in situ from smaller molecules and that the metabolic pathways for their formation are similar to those postulated by Kennedy and colleagues for the biosynthesis of phosphatides in chicken liver.The radioactivity of CMP-P32Ch also was incorporated into the phosphatides of homogenates of rat sciatic nerve. This incorporation was greater in homogenates prepared from nerves removed 13 days after previous section. It is suggested that these and other increases, found in the in vitro labelling of phosphatides in nerves degenerating after previous section, reported elsewhere, represent an increase in the potentiality of the nerve for remyelination. These increases are associated with the increase in the number of Schwann cells in the nerve.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

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.

The Natural Course of Defibrination Syndrome Caused by Echis Colorata Venom in Man

1974 ◽  
Vol 31 (03) ◽  
pp. 420-428 ◽  
Author(s):  
M Fainaru ◽  
S Eisenberg ◽  
N Manny ◽  
C Hershko
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Major Bleeding ◽  
Renal Damage ◽  
Specific Treatment ◽  
Natural Course ◽  
Factor V ◽  
Thrombocyte Count

SummaryThe natural course of defibrination syndrome caused by Echis colorata venom (ECV) in five patients is reported. All patients developed afibrinogenemia within six hours after the bite. Concomitantly a depression in factor V was recorded. Factor VIII and thrombocyte count in blood were normal in most patients. In the light of the known effects of ECV on blood coagulation in vivo and in vitro it is concluded that the afibrinogenemia is due to intravascular clotting.Four patients had transient renal damage, manifested by oliguria, azotemia, albuminuria and cylindruria, ascribed to microthrombi in the renal glomeruli.After the bite, the natural course was benign, no major bleeding was observed, and all signs of coagulopathy reverted to normal within 7 days. Therefore we recommend no specific treatment for this condition. In the case of heavily bleeding patients, administration of antiserum against ECV and/or heparin should be considered.

Effect of Temperature, Velocity Gradient and I.V. Heparin on in Vitro Blood Coagulation and Platelet Aggregation

1967 ◽  
Vol 17 (01/02) ◽  
pp. 112-119 ◽  
Author(s):  
L Dintenfass ◽  
M. C Rozenberg
Keyword(s):  
Blood Coagulation ◽  
Velocity Gradient ◽  
Elevated Temperatures ◽  
Morphological Changes ◽  
Effect Of Temperature ◽  
Clotting Time ◽  
Progressive Change ◽  
Aggregation Of Platelets ◽  
Microscopic Techniques

SummaryA study of blood coagulation was carried out by observing changes in the blood viscosity of blood coagulating in the cone-in-cone viscometer. The clots were investigated by microscopic techniques.Immediately after blood is obtained by venepuncture, viscosity of blood remains constant for a certain “latent” period. The duration of this period depends not only on the intrinsic properties of the blood sample, but also on temperature and rate of shear used during blood storage. An increase of temperature decreases the clotting time ; also, an increase in the rate of shear decreases the clotting time.It is confirmed that morphological changes take place in blood coagula as a function of the velocity gradient at which such coagulation takes place. There is a progressive change from the red clot to white thrombus as the rates of shear increase. Aggregation of platelets increases as the rate of shear increases.This pattern is maintained with changes of temperature, although aggregation of platelets appears to be increased at elevated temperatures.Intravenously added heparin affects the clotting time and the aggregation of platelets in in vitro coagulation.

Observations on the in vitro Effects of Chylomicra, Low-Density Lipoproteins and Phospholipids on Human Plasma Euglobulin Lysis

1963 ◽  
Vol 09 (01) ◽  
pp. 164-174 ◽  
Author(s):  
Albert R Pappenhagen ◽  
J. L Koppel ◽  
John H Olwin
Keyword(s):  
Human Plasma ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Inositol ◽  
Plasma Lipoproteins ◽  
Low Density ◽  
Inhibitory Effects ◽  
Soybean Phospholipids ◽  
In Vitro Effects ◽  
Complete Precipitation

SummaryData have been presented on the in vitro effects of human chylomicra, low-density human plasma lipoproteins, and partially purified preparations of various phospholipids on human plasma euglobulin lysis. Euglobulin lysis was found to be accelerated by preparations of mixed soybean phospholipids (aso-lectin), cephalin, phosphatidyl inositol, phophatidyl serine and phosphatidyl ethanolamine. In contrast, it was found to be inhibited by preparations of human chylomicra, low-density human plasma liproproteins and lecithin. Inhibition of euglobulin lysis produced by any of these three agents could be diminished or completely overcome by the simultaneous presence of suitable levels of any one of the accelerating agents. In all cases studied, both inhibitory and accelerating effects were observed to be concentration-dependent. Evidence has been obtained to suggest that in the case of the accelerating agents the observed increased rate of euglobulin lysis is not a direct effect on lysis itself, but rather is due to more complete precipitation of plasminogen in the presence of these substances. On the other hand, it appears that the inhibitory effects observed are not related to the extent of plasminogen precipitation, but are actually true inhibitions of euglobulin lysis. The possible clinical significance of some of these observations has been briefly discussed.

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