Acute Effects of Prostaglandin F2αon Ovarian and Luteal Blood Flow, Luteal Gonadotropin Uptakein Vivo,and Gonadotropin Bindingin Vitro*

Pang, Cho Y.; Behrman, Harold R.

doi:10.1210/endo-108-6-2239

Cited by 29 publications

(11 citation statements)

References 21 publications

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“…ROS generation by endothelial cells can be induced by ischemia-reperfusion through activation of the hypoxanthine-xanthine oxidase system, resulting in neutrophil activation and adhesion (8). In PGF 2␣ -induced luteolytic models, several experiments have shown that PGF 2␣ did not affect luteal hemodynamics in the early stage of luteolysis (5,14,22) and that xanthine oxidase activity in the rat corpus luteum did not change during PGF 2␣ -induced luteolysis (18). In our model, no significant microvascular hemodynamic alteration was noted during the 120-min observation period.…”

Section: Discussionmentioning

confidence: 43%

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats

Tanaka

Nishimura

Tanigaki

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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We investigated the contribution of neutrophils to prostaglandin (PG)F2α-induced luteolysis and the role of reactive oxygen species (ROS) as potential mediators of neutrophil accumulation in regressing corpora lutea of superovulated rats. On day 8of pseudopregnancy, subcutaneous injection of PGF2α (500 μg) significantly increased rhodamine 6G-labeled leukocyte adhesion in luteal venules, as observed by intravital microscopy. Neutrophil accumulation was confirmed by significantly increased myeloperoxidase (MPO) activity. Pretreatment with anti-leukocyte antibody (CD18-directed monoclonal antibody, WT-3) significantly inhibited the PGF2α-induced increases in adherent leukocytes and MPO activity. Anti-leukocyte antibody also maintained serum progesterone concentrations. Pretreatment with oxygen free radical scavengers, superoxide dismutase (50,000 U/kg) and catalase (90,000 U/kg), also attenuated these PGF2α-induced alterations. Corpora lutea preloaded with dichlorodihydrofluorescein diacetate succinimidyl ester, a fluorescent indicator for determining intracellular ROS generation, exhibited an increase in fluorescence after PGF2αtreatment. These findings suggest that leukocyte-endothelium interactions mediated by ROS generation are important in PGF2α-induced luteolysis in rats.

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Section: Discussionmentioning

confidence: 43%

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats

Tanaka

Nishimura

Tanigaki

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…Indeed, evidence is now accumulating that normal luteal regression in several species is not primarily ini¬ tiated by vascular mechanisms (sheep: EinerJensen & Mc Cracken 1976, 1977 guinea-pig: Hossain et al 1979;rat: Pang & Behrman 1979;Damber et al 1981). The well established luteolytic effect by prostaglandin F2a (PGF2a) in these species need not necessarily be mediated by a vascular action since it has been shown that PGF2a may act by interfering with the luteotrophic action of LH on luteal cells (Behrman & Hichens 1976;Pang & Behrman 1981).…”

Section: Direct Blood Flow Measurementsmentioning

confidence: 99%

Blood flow in the ovary and adjacent structures of the non-pregnant sheep

Janson¹,

Williams²,

Petrucco³

et al. 1983

Acta Endocrinologica

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Blood flow to the ovary, vascular pedicle and oviduct was measured in anaesthetized non-cycling and cycling ewes by timed collection of ovarian venous blood. The degree of arterio-venous shunting across the ovary and pedicle was estimated both in vivo and in vitro by perfusing the tissues with 15 \m=+-\5 \g=m\mradioactive micro\x=req-\ spheres.The mean ovarian blood flow in non-cycling animals was 1.9 ml/min, which was 51% of blood flow in the ovarian vein. In cycling animals ovarian blood flow at midcycle was 2.9 ml/min (66% of ovarian venous flow) in non\x=req-\ luteal ovaries and 4.3 ml/min (79% of venous flow) in luteal ovaries. The degree of arterio-venous shunting was low in all stages of the cycle (1.0\p=n-\2.6% across ovary + pedicle). The degree of shunting was also found to be very small in vitro (0.007\p=n-\1.38%) in both non-luteal and luteal ovaries. A considerable number of microspheres was entrapped in the vascular pedicle of the ovary indicating the presence of an extensive capillary bed. There was an inverse relationship between blood flow in the ovary and flow in the vascular pedicle.Alterations in distribution of blood flow between the ovary and adjacent structures supplied by the ovarian artery may be of functional significance in allowing rapid changes in ovarian blood flow. The results of the present study indicate that changes in ovarian blood flow during the oestrous cycle are not caused by an action on arteriovenous shunt vessels.In the search for mechanisms underlying the uter¬ ine control of corpus luteum (CL) function of the ewe, much attention has been paid to the structure of ovarian blood vessels and the rates of blood flow

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“…Macrophages and neutrophils, evident sources of oxygen radicals, are well documented to reside in both follicles and corpora lutea (10,(25)(26)(27)(28)(29). Both follicles and corpora lutea are also known to be subject to ischemic episodes (28,30), which may also release oxygen radicals. Oocytes of lower vertebrates generate oxygen radicals during formation of the fertilization envelope (31,32).…”

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confidence: 99%

Antigonadotropic and Antisteroidogenic Actions of Peroxide in Rat Granulosa Cells*

1990

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Reactive oxygen species are produced in the ovary. In luteal cells, peroxide abruptly inhibits LH-sensitive cAMP and progesterone production, and may serve a role as a mediator of luteolysis by such mechanisms. The objective of the present studies was to evaluate the acute actions of peroxide in rat granulosa cells. Peroxide at concentrations in the low micromolar range produced a marked and dose-dependent inhibition of FSH-sensitive cAMP accumulation and progesterone production, and depleted cell levels of ATP within 1 min. Longer treatment with peroxide (60 min) caused complete abrogation of the actions of FSH. Peroxide-induced depletion of ATP was prevented by 3-aminobenzamide, an inhibitor of DNA repair, but maintenance of cell levels of ATP did not prevent the anti-FSH effects of peroxide. Peroxide also abrogated cAMP accumulation and progesterone production in response to LH in granulosa cells. Unlike that seen with LH, inhibition of FSH-sensitive cyclic AMP accumulation by peroxide was partially reversed with isobutylmethyl xanthine, an inhibitor of cyclic AMP phosphodiesterase. Although peroxide inhibited cAMP accumulation in response to cholera toxin, it did not inhibit this same response to forskolin, which indicates that peroxide may interfere with G-protein-dependent activation of adenylate cyclase. Peroxide inhibited steroidogenesis in response to cholera toxin, forskolin, and 8-bromo-cAMP. The marked inhibitory actions of peroxide on gonadotropic hormone action and steroidogenesis in granulosa cells raise the possibility that peroxide may mediate events associated with loss of follicular function.

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Acute Effects of Prostaglandin F_2αon Ovarian and Luteal Blood Flow, Luteal Gonadotropin Uptakein Vivo,and Gonadotropin Bindingin Vitro*

Cited by 29 publications

References 21 publications

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats

Blood flow in the ovary and adjacent structures of the non-pregnant sheep

Antigonadotropic and Antisteroidogenic Actions of Peroxide in Rat Granulosa Cells*

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Acute Effects of Prostaglandin F2αon Ovarian and Luteal Blood Flow, Luteal Gonadotropin Uptakein Vivo,and Gonadotropin Bindingin Vitro*

Cited by 29 publications

References 21 publications

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F2α-induced luteolysis in rats

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F2α-induced luteolysis in rats

Blood flow in the ovary and adjacent structures of the non-pregnant sheep

Antigonadotropic and Antisteroidogenic Actions of Peroxide in Rat Granulosa Cells*

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Acute Effects of Prostaglandin F_2αon Ovarian and Luteal Blood Flow, Luteal Gonadotropin Uptakein Vivo,and Gonadotropin Bindingin Vitro*

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats

Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F_2α-induced luteolysis in rats