The influence of the phase of the estrous cycle on sheep endometrial tissue response to lipopolysaccharide.

The effect of lipopolysaccharide on ovine endometrial tissue was examined at estrus (follicular phase) and during the luteal phase. Endometrial tissues were cultured with 0, 1, or 10 microg/mL lipopolysaccharide. After 24 h, culture supernates were harvested and analyzed for PGF2alpha, PGE2, 6-keto-PGF1alpha, thromboxane B2 (TXB2), and cysteinyl-leukotrienes (leukotrienes) using EIA.

Endothelial vasodilator production by uterine and systemic arteries. IV. Cyclooxygenase isoform expression during the ovarian cycle and pregnancy in sheep.

Uterine artery endothelial production of the potent vasodilator, prostacyclin, is greater in pregnant versus nonpregnant sheep and in whole uterine artery from intact versus ovariectomized ewes. We hypothesized that uterine artery cyclooxygenase (COX)-1 and/or COX-2 expression would be elevated during pregnancy (high estrogen and progesterone) and the follicular phase of the ovarian cycle (high estrogen/low progesterone) as compared to that in luteal phase (low estrogen/high progesterone) or in ovariectomized (low estrogen and progesterone) ewes. Uterine and systemic (omental) arteries were obtained from nonpregnant luteal-phase (LUT; n = 10), follicular-phase (FOL; n = 11), and ovariectomized (OVEX; n = 10) sheep, as well as from pregnant sheep (110-130 days gestation; term = 145 +/- 3 days; n = 12).

The influence of reproductive phase on lipopolysaccharide stimulation of prostacyclin production and cyclooxygenase-2 protein concentrations in reproductive and systemic arteries of the sheep.

Cyclooxygenase, the enzyme that converts arachidonate to prostaglandins, plays a regulatory role in vasodilation under normal and pathological conditions. Studies were conducted to determine the effects of reproductive phase and lipopolysaccharide (LPS) on production of PGI2 and amounts of cyclooxygenase protein in uterine, mammary, mesenteric, and renal arteries. Arteries were collected from ewes during the follicular (Day 0 = estrus) or luteal (Day 10) phase of the estrous cycle and were cultured in the presence of LPS.

Cellular source in ewes of prostaglandin-endoperoxide synthase-2 in uterine arteries following stimulation with lipopolysaccharide.

Prostaglandin-endoperoxide synthase (PTGS) (also known as cyclooxygenase) converts arachidonic acid into several prostaglandins, many of which have roles in vasodilation and vasoconstriction under normal and pathological conditions. There are two isoforms of PTGS: PTGS-1 and PTGS-2; PTGS-1 is constitutively expressed in many tissues and is believed to be involved in the homeostatic maintenance of the body. In contrast, PTGS-2 is believed to have a "differentiative" role in the cells and is highly inducible during inflammation and in response to lipopolysaccharide (LPS).

Endothelial vasodilator production by uterine and systemic arteries. III. Ovarian and estrogen effects on NO synthase.

During the follicular phase of the ovarian cycle, when the local estrogen-to-progesterone ratio is elevated, uterine blood flow is elevated. This vasodilatory response is reproduced by exogenous 17beta-estradiol (E2beta) administration via a nitric oxide (NO)-mediated mechanism. We hypothesized that endogenous ovarian estrogen and exogenous E2beta treatment elevate expression of endothelial cell-derived NO synthase (eNOS) in uterine, but not in systemic, arteries.