Limit of detection: 80% B/B₀: 100 pg/ml · Sensitivity: 50% B/B₀: 400 pg/ml · Prostacyclin (Prostaglandin I₂; PGI₂) is formed from arachidonic acid primarily in the vascular endothelium and renal cortex by sequential activities of cyclooxygenase and PGI₂ synthase.^1,2 It is a potent vasodilator and inhibitor of platelet aggregation.² PGI₂ is non-enzymatically hydrated to 6-keto PGF_1α, and then quickly converted to the major urinary metabolite, 2,3-dinor-6-keto PGF_1α^3,4,5 Estimates of systemic PGI₂ production have often been assessed by measurement of 6-keto PGF_1α alone or in combination with 2,3-dinor-6-keto PGF_1α. However, the majority of 6-keto PGF_1α in urine is of renal origin with only 14% originating from plasma.^6,7 Cayman’s 2,3-dinor-6-keto PGF_1α EIA utilizes a highly selective monoclonal antibody that exhibits no cross reactivity with 6-keto PGF_1α, thus providing a method for accurate measurement of systemic PGI₂ production. These measurements are highly relevant to vascular biology research, especially as is relates to the elevated risk of myocardial infarction and stroke associated with the use of COX-2 selective inhibitors.^8,9

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).

8 Grosser, T., Fries, S., and Fitzgerald, G.A. Biological basis for the cardiovascular consequences of COX-2 inhibition: Therapeutic challenges and opportunities. J Clin Invest 116(1) 4-15 (2006).

9 Fitzgerald, G.A. Cardiovascular pharmacology of nonselective nonsteroidal anti-inflammatroy drugs and coxibs: Clinical considerations. Am J Cardiol 89 26D-32D (2002).

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).

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).

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

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

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).

Grosser, T., Fries, S., and Fitzgerald, G.A. Biological basis for the cardiovascular consequences of COX-2 inhibition: Therapeutic challenges and opportunities. J Clin Invest 116(1) 4-15 (2006).

Cheng, Y., Wang, M., Yu, Y., et al. Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function. J Clin Invest 2006 1-9 (2006).

Catella-Lawson, F., McAdam, B., Morrison, B.W., et al. Effects of specific inhibition of cyclooxygenase-2 on sodium balance, hemodynamics, and vasoactive eicosanoids. J Pharmacol Exp Ther 289(2) 735-741 (1999).

McAdam, B.F., Catella-Lawson, F., Mardini, I.A., et al. Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: The human pharmacology of a selective inhibitor of COX-2. Proc Natl Acad Sci USA 96 272-277 (1999).

Fitzgerald, G.A. Cardiovascular pharmacology of nonselective nonsteroidal anti-inflammatroy drugs and coxibs: Clinical considerations. Am J Cardiol 89 26D-32D (2002).

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

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).

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