scholarly journals In vitro effect of cinnamic aldehyde, a main component of Cinnamomi Cortex, on human platelet aggregation and arachidonic acid metabolism.

1987 ◽  
Vol 10 (5) ◽  
pp. 201-208 ◽  
Author(s):  
MITSUKO TAKENAGA ◽  
AIZAN HIRAI ◽  
TAKASHI TERANO ◽  
YASUSHI TAMURA ◽  
HARUO KITAGAWA ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Arachidonic Acid Metabolism ◽  
Cinnamic Aldehyde ◽  
Human Platelet Aggregation ◽  
Cinnamomi Cortex ◽  
Main Component ◽  
Vitro Effect

scholarly journals The influence of albumin and calcium on human platelet arachidonic acid metabolism

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 418-423 ◽  
Author(s):  
MJ Stuart ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Arachidonic Acid Metabolism ◽  
Albumin Concentration ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
External Calcium ◽  
Platelet Thromboxane

Abstract The effects of in vitro changes in calcium and albumin on human platelet arachidonic acid metabolism were evaluated. Hypoalbuminemia enhanced the conversion of released 14C-arachidonic acid from prelabeled platelet phospholipids to the metabolites of the platelet cyclooxygenase and lipoxygenase pathways. This effect was, however, associated with a decreased release of arachidonic acid in the presence of hypoalbuminemia, such that the overall conversion of released 14C- arachidonic acid to platelet thromboxane B2 was similar in the presence of physiologic albumin concentration (3.5 g/dl) or at decreased albumin concentrations of 0.7 and 0.0 g/dl. External calcium was shown to be important for optimal platelet arachidonic acid release, with maximal release occurring at 1 mM calcium.

scholarly journals The influence of albumin and calcium on human platelet arachidonic acid metabolism

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 418-423
Author(s):  
MJ Stuart ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Arachidonic Acid Metabolism ◽  
Albumin Concentration ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
External Calcium ◽  
Platelet Thromboxane

The effects of in vitro changes in calcium and albumin on human platelet arachidonic acid metabolism were evaluated. Hypoalbuminemia enhanced the conversion of released 14C-arachidonic acid from prelabeled platelet phospholipids to the metabolites of the platelet cyclooxygenase and lipoxygenase pathways. This effect was, however, associated with a decreased release of arachidonic acid in the presence of hypoalbuminemia, such that the overall conversion of released 14C- arachidonic acid to platelet thromboxane B2 was similar in the presence of physiologic albumin concentration (3.5 g/dl) or at decreased albumin concentrations of 0.7 and 0.0 g/dl. External calcium was shown to be important for optimal platelet arachidonic acid release, with maximal release occurring at 1 mM calcium.

In Vitro Effect Of Ticlopidine On Arachidonic Acid Metabolism In Platelet Phospholipids

1981 ◽  
Author(s):  
H Chap ◽  
M F Simon ◽  
L Douste-Blazy
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Maximum Effect ◽  
Prostaglandin D2 ◽  
Intact Cells ◽  
Vitro Effect ◽  
Slight Inhibition ◽  
Acylation Reactions

The effects of ticlopidine (Ti) on arachidonic acid (AA) metabolism in platelet phospholipids have been studied in vitro by following AA release from (14C) AA-prelabeled platelets or by measuring (14C)-AA incorporation into platelet phospholipids.In the presence of prelabeled platelets, Ti induced a release of AA essentially from phosphatidylcholine (PC) only at concentrations (10-3 M) where the drug became lytic. Incubation of cells previously lysed by sonication led to a deacylation of PC, part of the released AA being reincorporated into phosphatidylethanolamine (PE) . Under these conditions, Ti effect on PC disappeared and only a slight inhibition of AA incorporation into PE was observed.On the other hand, upon incubation of non-labeled platelets with (14C)-AA, Ti impaired the incorporation of AA into all platelet phospholipids, half maximum effect being observed under non-lytic conditions at 10-5-5.10-5 M.It is postulated that Ti inhibits the acylation reactions responsible for AA entry into glycerophospholipids. This effect might promote the release of trace amounts of AA in intact cells, which could explain the accumulation of stable, anti-aggregating prostaglandin D2 (M. Lagarde et al. Prostagl. Med. 1979, 2, 433).

Human Platelet Aggregation Induced by the Synthetic Endoperoxide Analogue U-46619 is Independent From Secretion, Prostaglandin Production and Extracellular Calcium

1979 ◽  
Author(s):  
G. Di Minno ◽  
L. Bianchi ◽  
G. de Gaetano ◽  
M.J. Silver
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Extracellular Calcium ◽  
Reversible Aggregation ◽  
Human Platelet Aggregation ◽  
Aspirin Ingestion

U-46619 is a stable analogue of cyclic prostaglandin endoperoxides which induces human platelet aggregation independently from nucleotide secretion. We studied platelet aggregation, 14C-5 HT release and malondialdehyde (MDA) production induced by this compound in stirred or unstirred platelet-rich plasma (PRP) samples from 11 healthy volunteers. Each subject was tested both before and 90 min after aspirin ingestion (500 mg). The threshold aggregating concentration (TAC) of U-466l9 ranged between 240 and 900 nM. Aggregation was maximal between 30 and 60 min after venepuncture and was concentration-dependent (60-7, 200nM). At concentrations below the TAC, U-466l9 induced primary reversible aggregation without detectable l4C-5 HT release. At TAC or higher concentrations aggregation and release proceeded as parallel events. Neither MOA production nor intracellular LDH loss could be detected in any of the tested situations. Aspirin ingestion did not modify the above pattern of platelet responses. In unstirred samples l4C - 5 HT release occurred to the same extent as in stirred platelet suspensions. Addition to citrated PRP of Na2 - EDTA did not affect either aggregation or release. It is suggested that aggregation and secretion may be independent, parallel responses of platelet activation by U-466l9 and do not require either extracellular calcium or activation of endogenous arachidonic acid metabolism. (Supported by the Italian CNR and NIH).

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