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P G Iatridis

Publications and source records attributed to P G Iatridis.

At least 19 recordsLinked to original sources
PubMed1987

Structure-function relationship of 3-phosphoglycerate analogues with platelet aggregation and thromboxane A2 formation.

We have studied the effects of 2,3-diphosphoglycerate (2,3-DPG), 3-phosphoglycerate (3-PG), 3-phosphoglyceraldehyde (3-PGA), 2-phosphoglycerate (2-PG) and beta-glycerol phosphate (beta-GP) on platelet aggregation and on thromboxane B2 (TXB2) formation. The results show that 2,3-DPG, 3-PG, and 3-PGA inhibited platelet aggregation and TXB2 formation induced by norepinephrine, ADP, epinephrine, and collagen; but they also induced platelet aggregation and TXB2 formation in the presence of subthreshold concentrations of Na arachidonate. 2-PG and beta-GP were inactive. The results also show that there is a structure-function relationship between 2,3-DPG, 3-PG, and 3-PGA with platelet aggregation phenomena and prostaglandin synthesis.

2,3-Diphosphoglycerate↗
PubMed1986

The combined effects of 2,3-DPG and Na-arachidonate on platelet aggregation and on TXA2 formation.

We have investigated the effects of 2,3-DPG on platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate by using the two cuvette transfer experiments of Hamberg, Svensson and Samuelsson (3). The results show that 2,3-DPG enhanced or induced platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate. Imidazole, a TXA2 synthetase inhibitor, and Lasix, when added inhibited 2,3-DPG effects on platelet aggregation, suggesting that 2,3-DPG may act either on cyclooxygenase or on TXA2 synthetase of prostaglandin synthesis. A specific RIA assay showed that 2,3-DPG when added to suboptimal concentrations of Na-Arachidonate enhanced the formation of TXB2, a stable metabolite of TXA2. We have concluded that during intravascular hemolysis 2,3-DPG release may be a key component in preventing and/or inducing thrombosis.

2,3-Diphosphoglycerate↗
PubMed1977

Thrombin-induced vasodilation in the hindlimb (dog).

The objective of this study is to test the hypothesis that the vasodilation produced by intra-arterial injection of thrombin to the hindlimb of a dog may be caused by the secondary release or production of some vasodilating substance. The vasodilator response to thrombin was compared with the vasodilator response to acetylcholine, isoproterenol, histamine and serotonin before and after blockade with atropine, propranolol, phenergan or methyl-D-lysergic acid butanolamide (UML-491), respectively. Though the appropriate blocking agent blocked the vasodilator response to the respective drug, the thrombin-induced vasodilation was not blocked. These data support the hypothesis that thrombin-induced vasodilation is a response to the thrombin moiety.

Acetylcholine↗
PubMed1976

Vasodilator effect of thrombins prepared from normal or deficient human or canine plasmas.

Thrombins prepared from plasmas deficient in various clotting factors are capable of inducing vasodilator response to the hindlimb of the dog and this response proved to be similar to that produced by thrombins prepared from normal plasmas. Thus the vascular effect of thrombin is not mediated by any other clotting factor which might be present in small amounts in the thrombin preparations. Thrombin prepared from canine normal plasma exerted a more potent vasodilator response, indicating a species specificity for the vascular response to thrombin. Since the vasodilating effect of thrombin is not mediated by (i) a nervous mechanism, (ii) any known vasodilating substance or (iii) any other clotting factor, it is concluded that the thrombin moiety possesses vasodilating properties.

Animals↗
PubMed1976

Stimulation of human platelet aggregation by phospholipase-A and a saline "extract" of a polyurethane.

A saline extract of polyurethane (SPU) induces enzymatic conversion of arachidonic acid (either exogenous or released through the action of exogenous phospholipase-A) by activating a hitherto undiscovered labile enzyme, synthetase-alpha which is not blocked by aspirin. Addition of SPU, plus arachidonic acid or SPU plus phospholipase-A to platelet-rich plasma (PRP) triggers a biphasic platelet aggregation. Incubation of SPU with PRP results in activation and exhaustion of synthetase-alpha; this renders platelets refractory to the various aggregating agents.

Aspirin↗
PubMed1975

2,3-diphosphoglycerate: a physiological inhibitor of platelet aggregation.

2,3-Diphosphoglycerate (2,3-DPG) may inhibit the platelet release reaction and the irreversible aggregation of human blood platelets induced by adenosine diphosphate, epinephrine, or norepinephrine. The effects of 2,3-DPG on platelet aggregation were more pronounced in cases with low hematocrit (less than 30 percent). Dipyridamole and vincaminor potentiated the antiaggregating effect of 2,3-DPG. Erythocytes (10-3 to 10-4 per microliter) exhibited a similar antiaggregating effect, especially when secured from anemic patients.

Adenosine Diphosphate↗