Search PubMed⌕ Search

Biomedical subjects

D Deykin

Publications and source records attributed to D Deykin.

140 records · Page 8Linked to original sources
PubMed1968

The incorporation of acetate and palmitate into lipids by human platelets.

The optimal conditions for the incorporation of acetate-1-(14)C and palmitic acid-1-(14)C into platelet lipids have been described. In buffer incubations with acetate there was a sharp pH optimum at 6.8; in plasma incubations, there was a broad pH optimum between 6.8-7.4. Maximal incorporation of acetate occurred at a final concentration of 1.5 mmoles/liter. In buffer, no labeled lipids were released from platelets into the medium. In plasma, 40% of newly formed lipids was recovered in the plasma. 75% of the incorporated acetate could be recovered in ceramide, lecithin, and free fatty acids. Platelet fatty acids were formed both by de novo synthesis and chain elongation. The fatty acids formed by de novo synthesis exchanged with plasma free fatty acids. In buffer incubations no turnover of newly labeled lipids occurred, but in the plasma incubations exchange of newly labeled lecithin with plasma lipids was demonstrable. Palmitic acid-1-(14)C added to plasma was incorporated into platelet lipids. The distribution among the lipid classes of palmitate taken up from plasma was the same as that of palmitate formed intracellularly by de novo synthesis.

Acetates↗
PubMed1967

Thrombogenesis.

Explore the source record for details and available documents.

Blood Coagulation↗
PubMedDate not supplied

Gelfoam and autologous clot embolization: effect on coagulation.

An episode of disseminated intravascular coagulation following therapeutic gelfoam embolization to control bleeding from esophageal varices in a patient with liver disease is presented. We have since followed 13 patients prospectively (six control and seven gelfoam/autologous clot) to determine the effect of this procedure on clotting. We were unable to show significant differences between the two groups as measured by the prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen and platelet count. However, fibrin (ogen) degradation products were significantly elevated (p less than .01) in the gelfoam/autologous clot group. We suspect this occurred secondary to clot lysis at the site of embolization. No subsequent bleeding diathesis attributable to this abnormality occurred in any of the patients.

Disseminated Intravascular Coagulation↗
PubMedDate not supplied

Passage state affects arachidonic acid content and eicosanoid release in porcine aortic endothelial cells.

Porcine aortic endothelial cells were cultured through four passages from primary cultures. The arachidonic acid content of individual phospholipid classes and the release of 6-keto-prostaglandin F1 alpha and 15-hydroxyeicosatetraenoic acid in response to 1 microM ionophore A23187 were assayed at each passage. The content of arachidonic acid in phosphatidylinositol and diacyl phosphatidylethanolamine remained constant at passage 1 but declined at passage 2 by approximately 29% and at passage 4 by approximately 59%. The release of 6-keto-prostaglandin F1 alpha was also unchanged at passage 1 but decreased by 60% at passage 2 and by 82% from its original value at passage 4. In contrast, the arachidonic acid content of diacyl phosphatidylcholine and of alkenyl phosphatidylethanolamine decreased with each passage, by 34% at passage 1, 59% at passage 2, 71% at passage 3, and 76% of the original value at passage 4. Stimulation with arachidonic acid reversed the passage effect. The release of 15-hydroxyeicosatetraenoic acid decreased by 82% at passage 1 and diminished to a 97% decrement from the original value by passage 4. When stimulated with arachidonic acid, 15-hydroxyeicosatetraenoic acid steadily decreased by approximately 70% at passages 3 and 4. The data indicate that passage state strikingly and nonuniformly affects phospholipid class arachidonic acid content and eicosanoid release in response to agonist stimulation.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Effect of chronic low dose aspirin on platelet and vascular eicosanoid metabolism in nonhuman primates (Macaca fascicularis).

It has been suggested that inhibition of platelet cyclooxygenase by chronic low dose aspirin may spare vascular prostacyclin production. Conventional doses of aspirin (greater than 5 mg/kg) have been shown to inhibit the generation of both thromboxane A2 and prostacyclin. Low dose aspirin inhibits prostacyclin production by excised human venous tissue, thus questioning the selectivity of such regimens. However, many clinical and surgical conditions requiring platelet inhibition involve the arterial system. We have studied the effects of various aspirin regimens on platelet, venous, and arterial cyclooxygenase activity in a nonhuman primate (Macaca fascicularis). We determined the lowest chronic dose of oral aspirin required to effectively inhibit platelet cyclooxygenase and aggregation to be 1 mg/kg. After 14 days of 0, 1, or 2 mg/kg aspirin, intact veins and arteries were surgically removed and perfused, and luminal prostacyclin (6-keto-PGF1 alpha) generation was assessed. Levels of 6-keto-PGF1 alpha in venous perfusates were reduced by 89% and 86% (p less than 0.05) after 1 and 2 mg/kg, respectively. Arterial 6-keto-PGF1 alpha levels were unchanged by 1 mg/kg aspirin, but after 2 mg/kg were reduced by 66% (p less than 0.05). Preferential inhibition of platelet over arterial cyclooxygenase is thus achievable, but only over a narrow dose range.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Interaction of ethanol, prostacyclin, and aspirin in determining human platelet reactivity in vitro.

Ethanol partitions into cellular membranes and alters membrane-associated phenomena in numerous cell types. Since platelet aggregation and its inhibition by prostacyclin are mediated by membrane-associated receptors and enzymes, we examined the interaction of ethanol, prostacyclin, and aspirin on human platelet reactivity. Using platelet-rich plasma, we examined the effect of increasing concentrations of ethanol (0.05% to 1.0%) on the platelet-inhibitory effects of a submaximal dose (5 x 10(-10) M) of prostacyclin, the concomitant production of cyclic 3',5'-adenosine monophosphate (AMP), and the release of thromboxane A2. Ethanol alone had little effect on platelet aggregation induced by 5 micrograms/ml collagen; however, it potentiated the inhibitory effect of prostacyclin on platelet aggregation in a dose-dependent manner in the range of 0.05% to 1.0% ethanol. Whereas prostacyclin increased platelet cyclic AMP levels, ethanol had no further effect on cyclic AMP levels. Ethanol alone reduced thromboxane A2 generation, but this effect could not totally account for the observed interaction of ethanol and prostacyclin on aggregation, since aspirin did not totally abolish the interaction. The dose range in which the ethanol/prostacyclin/aspirin interactions occur encompasses the plasma levels of ethanol that may be achieved by the consumption of alcoholic beverages. The results may, in part, explain the dose-related physiological and pathological consequences of chronic alcohol consumption on the cardiovascular system.

Aspirin↗