Thromboxane B2, 6-keto-PGF1α, PGE2, PGF2α, and PGA1 plasma levels in arteriosclerosis obliterans: Relationship to clinical manifestations, risk factors, and arterial pathoanatomy

Jouve, R; Rolland, Pierre H.; Delboy, C; Mercier, C

doi:10.1016/0002-8703(84)90132-7

Cited by 40 publications

(14 citation statements)

References 32 publications

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“…15 Direct in vivo assay of PGI 2 formation by atherosclerotic arteries is not currently possible and, thus, other authors have investigated endogenous PGI 2 synthesis by indirect methods. 15 ' 16 Basal production of PGI 2 under physiologic conditions is reported to be low. Patients with severe atherosclerosis and evidence of platelet activation were observed to excrete higher urinary levels of 2,3-dinor-6-keto-PGF la (one of a number of in vivo PGI 2 metabolites) than normal subjects; 15 these authors concluded that reduced PGI 2 formation by atherosclerotic specimens observed in vitro was, therefore, physiologically irrelevant.…”

Section: Discussionmentioning

confidence: 99%

Prostacyclin, thromboxane A2, and prostaglandin E2 formation in atherosclerotic human carotid artery.

et al. 1988

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Prostaglandin (PG) formation In 16 atherosclerotic human carotid endarterectomy specimens was compared systematically with that of normal carotid artery from seven white pigs and six rhesus monkeys. Prostacyclin (PGI2) formation (plcomoles 6-keto-PGF 1t /2 mln/100 ^9 homogenate protein plus 2 mM glutathlone [GSH]) of nonatheromatous Intlma adjacent proximal (276 ± 32, mean ± SEM) or distal (271 ± 14) to carotid plaque was comparable to that of normal carotid artery from white pig (272 ± 25, NS) and rhesus monkey (219 ± 41, NS), and was greater than stenotlc Intlma (156 ± 1 7 , p<0.01), sublntlmal plaque (168 ± 14, p < 0.01), and ulceratlon (65 ± 16, p<0.01 A rterial prostaglandin (PG) synthesis Is thought to be important in the maintenance of circulatory homeostasis by contributing to regulation of vascular tone and endothelial platelet adherence. Prostacyclin (PGy, the major product of arachidonic acid metabolism in normal vascular endothelium, is a potent vasodilator and inhibitor of platelet aggregation and adherence to the vessel wall. 1It has been hypothesized that PGI 2 counterbalances the proaggregatory and vasoconstrictive effects of predominantly platelet-synthesized thromboxane Aj (TXAj).1 Recent reports 2 ' 3 -4 suggest that atherosclerotic arteries differ from normal arterial tissues by producing substantially less PGI 2 , more PGE 2 , 4 and detectable levels of TXA 2 . 5 Such alterations in PG synthesis could create a localized imbalance between the intravascular actions of PGI 2 and TXAa, resulting in increased platelet deposition and arterial thrombogenicity at atherosclerotic sites.The underlying biochemical basis for reported alterations in arterial PG synthesis in atherosclerosis is unclear. Furthermore, it has not been demonstrated whether such changes in atherosclerotic patients are focal (localized only to plaque) or systemic (also found in nonatheromatous arterial tissues). The purpose of this study was to identify enzymatic changes in carotid endarterectomy Received May 26,1987; revision accepted September 9,1987. specimens that might account for these previously observed disturbances of eicosanoid metabolism and investigate the potential of glutathione (GSH), an endogenous antioxidant, to modulate PG synthesis. Methods Normal Carotid Artery SpecimensA single specimen of nonatherosclerotic human carotid artery (n = 1) was harvested with appropriate authorization from a brain-dead cadaver kidney donor. Fresh carotid arteries from young adult, white (cross-bred, market grade) pigs (n = 7) and rhesus monkeys (n = 6) were used as control specimens. The animal experiments conformed to principles of animal care established by the Tulane Medical Center Advisory Committee for Animal Resources, "Principles of Laboratory Animal Care," and the "Guide for the Care and Use of Laboratory Animals" (NIH publication No. 80-23, revised 1978). Atherosclerotic Carotid Artery SpecimensOcclusive atheromatous internal carotid artery plaques were removed from patients (n = 16) by standard carotid endarterecto...

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Section: Discussionmentioning

confidence: 99%

Prostacyclin, thromboxane A2, and prostaglandin E2 formation in atherosclerotic human carotid artery.

et al. 1988

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“…The stable metabolites thromboxane and prostacyclin are imbalanced in arteriosclerotic lesions in patients and animal models. An abnormally high level of TXB2 in plasma was reported in patients with atherosclerosis obliterans and was positively correlated with serum triglyceride content and vascular injury index [30]. TBXAS1 was found increased in level in blood vessels and induced vasoconstriction and platelet activation [29].…”

Section: Discussionmentioning

confidence: 97%

Metabolomic analysis revealed the role of DNA methylation in the balance of arachidonic acid metabolism and endothelial activation

Xue

Zhang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…13 Informed consent was obtained. Blood samples were drawn from the midstream of a brachial vein by careful venipuncture after stasis of less than 10 seconds, using a siliconized 18-gauge needle.…”

Section: Platelet Collection and Processingmentioning

confidence: 99%

“…This restricted inhibition of platelet activities by ISDN may explain, at least in part, why in previous studies the absence of changes in platelet aggregation has been noted under organic therapy. 9 To explain why the minimal nitrate concentration inhibiting platelet aggregation is much lower in vitro than in vivo, it has been proposed that organic nitrates may stimulate the production of prostacyclin (PGI), an antiaggregating and vasodilatory substance generated by the endothelium, 611 " 13 which in turn decreases vascular tone and inhibits platelet activity. 1415 It is now generally acknowledged that the stimulating effect of nitrates on PGI 2 production is not likely to account for the vasodilation properties of these drugs.…”

mentioning

confidence: 99%

Antithrombogenic endothelial cell defense. Basal characteristics in cultured endothelial cells and modulation by short-term and long-term exposure to isosorbide nitrates.

Berenger¹,

Cano²,

Rolland³

1987

Circulation Research

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The antithrombogenic endothelial cell defense (ATECD) describes the properties that enable the endotheliiim to prevent circulating blood platelets from adhering to, or aggregating on, the vascular wall. ATECD was investigated in an experimental model in which bovine passage 0 cultured endotheli-al cells (EC) were incubated with aggregating platelets and autologous plasma in a computer-operated aggregometer-like device. A maximal platelet aggregation required 150 x 10-* M adenosine diphos-phate (ADP) to be present in ECs. A 5-minute coincubation for ECs and platelets was found to be adequate in evaluating the maximal ATECD value. By increasing the EC number in the aggregation suspension, platelet aggregation was progressively inhibited through a signioid curve (50% inhibition of aggregation required 2 x 10 4 EC). Pharmacologic modulations of ATECD by isosorbide dinitrate (ISDN) + 2-isosorbide mononitrate (2-ISMN) + 5-isosorbide mononitrate (5-ISMN) were investigated under experimental conditions reflecting either an acute nitrate effect (platelet + control ECs + drug + ADP) or a chronic effect (platelet + 5-day nitrate-treated ECs + ADP). Under acute circumstances, ISDN antiplatelet activities were profoundly magnified by ECs. Aggregation was fully arrested with 5 X 10~ 5 M ISDN and an EC number of 2 x 10 4 , whereas the same ISDN concentration alone induced 30% inhibition of control aggregation. In contrast, there were no significant changes in platelet aggregation whether incubation was done in the presence or absence of 2-ISMN or 5-ISMN, ISDN metabolites. Long-term exposure of ECs to isosorbide nitrates (ISN) resulted in increased acquired EC changes in ATECD. 5-ISMN was a poor antiplatelet agent but was capable of counteracting ISDN effects on ATECD. Under chronic circumstances, the overall ISN effect was a stimulation of ATECD, but the final effect was lower than that expected from the summation of individual ISN effects. Such an endotheliuni-dependent ISDN (and perhaps 2-ISMN) antiplatelet activity is likely to explain why ISDN inhibits platelet activity in vivo, while in vitro, ISDN fails to elicit such platelet aggregation inhibition unless suprapharmacologic ISDN concentrations are used. It is suggested that pharmacologic modulation of ATECD may be a new antithrombotic therapy. (Circulation Research 1987;60:612-620)

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Thromboxane B2, 6-keto-PGF1α, PGE2, PGF2α, and PGA1 plasma levels in arteriosclerosis obliterans: Relationship to clinical manifestations, risk factors, and arterial pathoanatomy

Cited by 40 publications

References 32 publications

Prostacyclin, thromboxane A2, and prostaglandin E2 formation in atherosclerotic human carotid artery.

Prostacyclin, thromboxane A2, and prostaglandin E2 formation in atherosclerotic human carotid artery.

Metabolomic analysis revealed the role of DNA methylation in the balance of arachidonic acid metabolism and endothelial activation

Antithrombogenic endothelial cell defense. Basal characteristics in cultured endothelial cells and modulation by short-term and long-term exposure to isosorbide nitrates.

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