Enzyme immunoassay measurement of the urinary metabolites of thromboxane A2 and prostacyclin

Lellouche, Franck; Fradin, Armel; FitzGerald, Garret A.; Maclouf, Jacques

doi:10.1016/0090-6980(90)90017-p

Cited by 51 publications

(25 citation statements)

References 14 publications

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“…Previously, 6-keto-PGF 1␣ was assumed to be an inactive, nonenzymatic hydrolysis product of prostacyclin, an unstable prostanoid derived from the COXs (46). Given their stability under physiologic conditions, 6-keto-PGF compounds have been used extensively as a urinary marker of endothelial activation in vivo (47). For example, the fate of labeled prostacyclin in humans was examined and revealed that all identified metabolites were of the 6-keto-PGF structure (32).…”

Section: Discussionmentioning

confidence: 99%

Activated endothelial cells elicit paracrine induction of epithelial chloride secretion. 6-Keto-PGF1alpha is an epithelial secretagogue.

Blume

Taylor²,

Lennon³

et al. 1998

J. Clin. Invest.

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Endothelial cells play a central role in the coordination of the inflammatory response. In mucosal tissue, such as the lung and intestine, endothelia are anatomically positioned in close proximity to epithelia, providing the potential for cell-cell crosstalk. Thus, in this study endothelial-epithelial biochemical crosstalk pathways were studied using a human intestinal crypt cell line (T84) grown in noncontact coculture with human umbilical vein endothelia. Exposure of such cocultures to endothelial-specific agonists (LPS) resulted in activation of epithelial electrogenic Cl Ϫ secretion and vectorial fluid transport. Subsequent experiments revealed that in response to diverse stimuli (LPS, IL-1 ␣ , TNF-␣ , hypoxia), endothelia produce and secrete a small, stable epithelial secretagogue into conditioned media supernatants. Further experiments identified this secretagogue as 6-keto-PGF 1 ␣ , a stable hydrolysis product of prostacyclin (PGI 2 ). Results obtained with synthetic prostanoids indicated that 6-keto-PGF 1 ␣ (EC 50 ϭ 80 nM) and PGI 2 stable analogues (EC 50 ϭ 280 nM) activate the same basolaterally polarized, Ca 2 ϩ -coupled epithelial receptor. In summary, these findings reveal a previously unappreciated 6-keto-PGF 1 ␣ receptor on intestinal epithelia, the ligation of which results in activation of electrogenic Cl Ϫ secretion. In addition, these data reveal a novel action for the prostacyclin hydrolysis product 6-keto-PGF 1 ␣ and provide a potential endothelialepithelial crosstalk pathway in mucosal tissue. ( J. Clin. Invest. 1998. 102:1161-1172.)

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Section: Discussionmentioning

confidence: 99%

Activated endothelial cells elicit paracrine induction of epithelial chloride secretion. 6-Keto-PGF1alpha is an epithelial secretagogue.

Blume

Taylor²,

Lennon³

et al. 1998

J. Clin. Invest.

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“…In order to study whether the synthesis of the vasodilator prostanoid PGI 2 could be altered after chronic treatment of the rats with L-NAME, the concentration of 6-keto-PGF 1· , a stable metabolite of PGI 2 of vascular origin [22], was measured in plasma. NR and LHR blood samples were collected in tubes containing EDTA and indomethacin, centrifuged, and plasma samples were store at -20°C until the assay was conducted.…”

Section: Effect Of Treatment With L-name For 3 Weeks Upon Contractionsmentioning

confidence: 99%

Functional Study of the [Ca2+]i Signaling Pathway in Aortas of L-NAME-Hypertensive Rats

Grifoni

Bendhack²

2004

Pharmacology

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A variety of mechanisms has been proposed to suggest that nitric oxide participates in the regulation of smooth muscle free [Ca²⁺]_c (the primary determinant of contractile tone), including inhibition of Ca²⁺ influx across the plasma membrane and inhibition of intracellular Ca²⁺ release. In view of such considerations, the aim of this study was to investigate the possible alterations in contractile responses induced by drugs that mobilize Ca²⁺ from different sources in aortae from N^G-nitro-L-arginine methyl ester (L-NAME) hypertensive rats (LHR). Treatment with L-NAME did not alter the contractile response induced by phenylephrine; however, indomethacin increased the contraction to phenylephrine only in LHR aortae (1.36 ± 0.08 g, n = 6, vs. 1.97 ± 0.09 g, n = 7). Both phenylephrine and caffeine evoked rapid and phasic contractions in intact or denuded aortic rings in Ca²⁺-free solution containing EGTA. Phenylephrine-elicited phasic contractions were lower in normotensive rats (NR; 0.41 ± 0.05 g, n = 9) than in LHR (0.57 ± 0.06 g, n = 6) and were increased by endothelium removal only in the NR group (0.64 ± 0.05 g, n = 6). Conversely, neither with treatment with L-NAME nor endothelium removal altered the phasic contractile responses induced by caffeine. The Ca²⁺ influx stimulated with phenylephrine was greater in NR (1.95 ± 0.08 g; pD₂ 6.06 ± 0.69; n = 8) than in the LHR denuded aorta (1.63 ± 0.11 g; pD₂ 3.52 ± 0.06; n = 6). Similarly, contractions stimulated with phorbol ester in denuded arteries were greater in NR (1.76 ± 0.08 g, n = 7) than in LHR (1.11 ± 0.11 g, n = 7). In the same manner, indomethacin failed to alter the contraction stimulated with phorbol ester in NR arteries (2.01 ± 0.21 g, n = 7), although it completely blocked the inhibitory effect of chronic treatment with L-NAME on this contractile response (1.94 ± 0.24 g; n = 9). Indomethacin did not change the contractile responses stimulated by increasing concentrations of extracellular Ca²⁺ in either NR aortas (1.44 ± 0.26 g; pD₂ 4.74 ± 0.79; n = 6) or LHR aorta (1.99 ± 0.19 g; pD₂ 4.10 ± 0.47; n = 8). However, in the presence of indomethacin, the Ca²⁺ influx was similar in NR and LHR aortae. Taken together, these results suggest that, in this model of hypertension, the increase in agonist-induced release of Ca²⁺ from intracellular stores may be partly compensated by inhibition of Ca²⁺ influx and that this effect is due to the increased production of the relaxant prostanoid in vascular smooth muscle cells.

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“…Afterwards the specimen was centrifuged (3000Âg, 10 min, 48C), and the supernatant frozen at À708C for further analysis. Serum TXB 2 was measured by previously validated enzyme-linked immunoassay techniques (Cayman Chemical Company, Ann Arbor, Michigan, USA, sensitivity 0.004 ng/ml for TXB 2 ) [15,16] ROS was studied with the use of total oxidative plasma status and total antioxidative capacity of the plasma was also measured. The total oxidative plasma status was estimated with the use of PerOx (TOS) kit by Immundiagnostik AG (Bensheim, Germany) measuring total lipid peroxides.…”

Section: Methodsmentioning

confidence: 99%

Relationship between high on aspirin platelet reactivity and oxidative stress in coronary artery by-pass grafted patients

Kuliczkowski¹,

Golański

Bijak

et al. 2016

Blood Coagulation &Amp; Fibrinolysis

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The aim of the study was to assess the responsiveness of blood platelets to acetylsalicylic acid (ASA) in patients following coronary artery bypass grafting (CABG) surgery with relation to oxidative and antioxidative plasma status. The study included 37 patients treated with the CABG procedure. During the first 24 h after CABG patients were given 300 mg of ASA with the following dose of 150 mg daily. The blood was collected before the procedure and 10 days after. Whole blood platelet aggregation induced with arachidonic acid, collagen and adenosine diphosphate (ADP) was performed together with whole blood generation of thromboxane B2 (TxB2). Oxidative stress was measured before and 10 days after CABG with total oxidative plasma status (TOS) and total antioxidative status of the plasma (TAS). TOS/TAS index was calculated. We observed a significant increase in the TOS and TOS/TAS index and ADP-induced aggregation 10 days after CABG in comparison with its level before operation. There was a significant decrease in the arachidonic acid-induced aggregation and serum TxB2 level. Patients with ADP-induced and collagen-induced aggregation in the upper quartile had significantly higher TOS and TOS/TAS index before (ADP) and after the operation (ADP and collagen). There were 19 patients (51%) with high on aspirin platelet reactivity after CABG who had also higher TOS and TOS/TAS index and lower TAS value in comparison with aspirin responders. Despite ASA use, increased oxidative stress after CABG can overcome its antiplatelet effect and increase platelet activation through other pathways.

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Enzyme immunoassay measurement of the urinary metabolites of thromboxane A2 and prostacyclin

Cited by 51 publications

References 14 publications

Activated endothelial cells elicit paracrine induction of epithelial chloride secretion. 6-Keto-PGF1alpha is an epithelial secretagogue.

Activated endothelial cells elicit paracrine induction of epithelial chloride secretion. 6-Keto-PGF1alpha is an epithelial secretagogue.

Functional Study of the [Ca<sup>2+</sup>]<sub>i</sub> Signaling Pathway in Aortas of <i>L</i>-NAME-Hypertensive Rats

Relationship between high on aspirin platelet reactivity and oxidative stress in coronary artery by-pass grafted patients

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