Limit of detection: 80% B/B₀: 6 pg/ml · Sensitivity: 50% B/B₀: 40 pg/ml · Prostacyclin (Prostaglandin I₂; PGI₂) is formed from arachidonic acid primarily by the vascular endothelium and renal cortex.^1,2 It is a potent vasodilator and inhibitor of platelet aggregation.² PGI₂ is non-enzymatically hydrated to 6-keto PGF_1α (t1/2 = 2-3 minutes), and then quickly converted to the major metabolite, 2,3-dinor-6-keto PGF_1α (t1/2 = 30 minutes).^3,4,5 Prostacyclin was once thought to be a circulating hormone that regulated platelet-vasculature interactions, but the rate of secretion into circulation coupled with the short half-life indicate that prostacyclin functions locally.⁶ Although 6-keto PGF_1α is commonly measured in plasma and urine as an estimate of prostacyclin synthesis, it should be noted that there may be more than one source of PGI₂ in these samples. For instance, venipuncture may cause the release of prostacyclin which will artifactually increase the 6-keto PGF_1α concentration in plasma.⁷ Urinary concentrations of 6-keto PGF_1α are confounded by the fact that some plasma prostacyclin (~14%) is excreted into urine as 6-keto PGF_1α and the remainder is of renal origin.^6,7 Therefore, it is important to take these factors into account when analyzing data.

1 Moncada, S., Gryglewski, R., Bunting, S., et al. An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation. Nature 263 663-665 (1976).

2 Navamani, M., Morgan, M., and Williams, R.J. Ethanol modulates N-methyl-D-aspartate-evoked arachidonic acid release from neurones. Eur J Pharmacol 340 27-34 (1997).

3 Samuelsson, B., Goldyne, M., Granström, E., et al. Prostaglandins and thromboxanes. Annu Rev Biochem 47 997-1029 (1978).

4 Dusting, G.J., Moncada, S., and Vane, J.R. Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachidonic acid. Prostaglandins 13 3-15 (1977).

5 Rosenkranz, B., Fischer, C., Reimann, I., et al. Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F_1α in man. Biochim Biophys Acta 619 207-213 (1980).

6 Frolich, J.C. Measurement of eicosanoids. Prostaglandins 27 349-369 (1984).

7 Catella, F., Nowak, J., and Fitzgerald, G.A. Measurement of renal and non-renal eicosanoid synthesis. Am J Med 81 23-29 (1986).

Samuelsson, B., Goldyne, M., Granström, E., et al. Prostaglandins and thromboxanes. Annu Rev Biochem 47 997-1029 (1978).

Frolich, J.C. Measurement of eicosanoids. Prostaglandins 27 349-369 (1984).

Rosenkranz, B., Fischer, C., Reimann, I., et al. Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F_1α in man. Biochim Biophys Acta 619 207-213 (1980).

Moncada, S., Gryglewski, R., Bunting, S., et al. An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation. Nature 263 663-665 (1976).

Westcott, J.Y., Chang, S., Balazy, M., et al. Analysis of 6-keto PGF_1α, 5-HETE, and LTC₄ in rat lung: Comparison of GC/MS, RIA, and EIA. Prostaglandins 32 857-873 (1986).

Cott, G.R., Westcott, J.Y., and Voelkel, N.F. Prostaglandin and leukotriene production by alveolar type II cells in vitro. Am J Physiol 258 L179-L187 (1990).

Westcott, J.Y., Murphy, R.C., and Stenmark, K. Eicosanoids in human ventricular cerebrospinal fluid following severe brain injury. Prostaglandins 34 877-887 (1987).

Maxey, K.M., Maddipati, K.R., and Birkmeier, J. Interference in enzyme immunoassays. J Clin Immunoassay 15 116-120 (1992).

Pradelles, P., Grassi, J., and Maclouf, J.A. Enzyme immunoassays of eicosanoids using acetylcholinesterase as label: An alternative to radioimmunoassay. Anal Chem 57 1170-1173 (1985).

Davidge, S.T., Baker, P.N., McLaughlin, M.K., et al. Nitric oxide produced by endothelial cells increases production of eicosanoids through activation of prostaglandin H synthase. Circ Res 77 274-283 (1995).

Traverse, J.H., Judd, D., and Bache, R.J. Dose-dependent effect of endothelin-1 on blood flow to normal and collateral-dependent myocardium. Circulation 93 558-566 (1996).

Marshall, L.A., Bolognese, B., Winkler, J.D., et al. Depletion of human monocyte 85-kDa phospholipase A₂ does not alter leukotriene formation. J Biol Chem 272 759-765 (1997).

Thibodeaux, J.K., Broussard, J.R., Godke, R.A., et al. Stimulation of progesterone production in bovine luteal cells by co-incubation with bovine blastocyst-stage embryos or trophoblastic vesicles. J Reprod Fertil 101 657-662 (1994).

Salvemini, D., Settle, S.L., Masferrer, J.L., et al. Regulation of prostaglandin production by nitric oxide; an in vivo analysis. Br J Pharmacol 114 1171-1178 (1995).

Schramm, D.D., Pearson, D.A., and German, J.B. Endothelial cell basal PGI₂ release is stimulated by wine in vitro: One mechanism that may mediate the vasoprotective effects of wine. J Nutr Biochem 8 647-651 (1997).

Lellouche, F., Fradin, A., FitzGerald, G., et al. Enzyme immunoassay measurement of the urinary metabolites of thromboxane A₂ and prostacyclin. Prostaglandins 40 297-310 (1990).

Berg, J., Christoph, T., Widerna, M., et al. Isoenzyme-specific cyclooxygenase inhibitors: A whole cell assay system using the human erythroleukemic cell line HEL and the human monocytic cell line Mono Mac 6. J Pharmacol Toxicol Methods 37 179-186 (1997).

Catella, F., Nowak, J., and Fitzgerald, G.A. Measurement of renal and non-renal eicosanoid synthesis. Am J Med 81 23-29 (1986).

Li, J., Oliver, J.R., Lu, C., et al. Delayed thromboxane or tumor necrosis factor-α, but not leukotriene inhibition, attenuates prolonged pulmonary hypertension in endotoxemia. Am J Med Sci 310 103-110 (1996).

Navamani, M., Morgan, M., and Williams, R.J. Ethanol modulates N-methyl-D-aspartate-evoked arachidonic acid release from neurones. Eur J Pharmacol 340 27-34 (1997).

Maclouf, J., Grassi, J., and Pradelles, P. Development of enzyme-immunoassay techniques for the measurement of eicosanoids. 355-364 (1987).

Muth-Selbach, U.S., Tegeder, I., Brune, K., et al. Acetaminophen inhibits spinal prostaglandin E₂ release after peripheral noxious stimulation. Anesthesiology 91 231-239 (1999).

Dusting, G.J., Moncada, S., and Vane, J.R. Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachidonic acid. Prostaglandins 13 3-15 (1977).

Gurbel, P.A., Murugesan, S.R., Lowry, D.R., et al. Plasma thromboxane and prostacyclin are linearly related and increased in patients presenting with acute myocardial infarction. Prostaglandins Leukot Essent Fatty Acids 61 7-11 (1999).

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