Ovarian capillary blood flow in seasonally anoestrous ewes induced to ovulate by treatment with GnRH

Brown, B. W.; Cognie, Y.; Chemineau, Philippe; Poulin, Noëlle; Salama, O. A.

doi:10.1530/jrf.0.0840653

Cited by 5 publications

(2 citation statements)

References 4 publications

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“…Hence, inhibitory effects on ovulation induced by the use of NOS inhibitors may be due to inhibition of NO-derived relaxation of ovarian vascular smooth muscle and unmasking of the vasopressor response to endothelin [35], leading to decreases in ovarian blood flow or, in the case of the in vitro-perfused ovaries, decreases in perfusate flow. Ovarian blood flow normally increases as ovulation approaches [36,371 and contributes to the hyperemia and macroscopically observable "follicular blushing" that accompany the general increase in vascular permeability and edema observed in ovulating ovaries. By comparing the flow rates of LH-perfused and LH + L-NAME-perfused ovaries we have shown that there is an approximately 46% decrease in flow rate upon addition of the NOS inhibitor at a dose of 3.5 X 10 -5 mol/L; as mimicked in optimally stimulated ovaries, this resulted in a decreased ovulation rate that accounted for approximately 76% of the effect observed in this group when perfused with L-NAME.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Nitric Oxide: Effects on Interleukin-lβ-Enhanced Ovulation Rate, Steroid Hormones, and Ovarian Leukocyte Distribution at Ovulation in the Rat1

Bonello

McKie

Jasper

et al. 1996

Biology of Reproduction

162

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The ovulatory process resembles an inflammatory reaction with an infiltration of leukocytes, production of inflammatory mediators such as cytokines, and a general edema and hyperemia. Nitric oxide (NO), a potent vasodilator and the main mediator of macrophage tumoricidal and bacteriocidal activities, is known to participate in inflammatory reactions and has been shown to mediate the interleukin-1 beta (IL-1 beta)-directed tissue-remodeling events within the ovary. The regulation by NO of ovulation rate, leukocyte distribution, and steroid release in the rat ovary was investigated through use of a combination of in vivo and in vitro models of ovulation and a competitive inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), of the NO synthase (NOS) enzyme. Subcutaneous L-NAME (1.5 x 10(-4) mol/kg) administration significantly reduced the in vivo ovulation rate of eCG/hCG-primed rats (L-NAME-treated: 10.6 +/- 1.8 [mean +/- SEM] oocytes per ovary [O/O], 11.0 +/- 1.2 rupture sites per ovary [RS/O]; saline-treated: 18.0 +/- 1.8 O/O, 19.4 +/- 1.1 RS/O; p < 0.01) at 20 h post-hCG. These results were reflected in vitro, where addition of L-NAME (3.5 x 10(-5) mol/L) to LH (0.1 microgram/ml)-perfused ovaries decreased ovulation rate from 8.2 +/- 1.6 to 2.7 +/- 1 ovulations per ovary (p < 0.05) and simultaneously decreased nitrite accumulation at the completion of perfusions from 16.5 +/- 1.9 to 4.1 +/- 0.5 nmol/ml (p < 0.001). The addition of L-NAME to LH+IL-1 beta (4 ng/ml)-perfused ovaries decreased ovulation rate from 15.2 +/- 2.4 to 0.8 +/- 0.8 ovulations per ovary (p < 0.001) and simultaneously decreased nitrite accumulation at 22 h from 22.8 +/- 2.2 to 1.9 +/- 0.6 nmol/ml (p < 0.001). Studies analyzing and manipulating perfusion flow rate indicated that the L-NAME effects on ovulation rate are primarily due to a reduction in flow rate resulting from inhibition of NO, which may be a consequence of the known vasoconstrictor effects of NOS inhibitors. The observed reduction of in vivo ovulation rate by NO inhibition at 20 h post-hCG was associated with a significant reduction in thecal MCA149+ neutrophils at 12 h post-hCG, the expected time of ovulation (L-NAME-treated: 98.4 +/- 9.2 cells per thecal area; saline-treated: 211.5 +/- 11.5 cells per thecal area; p < 0.001), while ED1+ monocytes/macrophages underwent similar but nonsignificant changes. Plasma (20 h post-hCG) and perfusate progesterone were not different with L-NAME treatment, while perfusate estradiol levels were markedly reduced upon addition of L-NAME, suggesting a role for NO in ovulation but not in the process of luteinization. In summary, deprivation of NO by use of the competitive inhibitor, L-NAME, led to fewer ovulations, reduced accumulation of nitrite, a decreased neutrophil count in the theca of preovulatory follicles, and reduced estradiol secretion, while progesterone release remained unaffected. The NO pathway may therefore play an important role in the regulation of ovulation and the mediation of IL-1 beta's pro-ovulatory effects. There ar...

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Section: Discussionmentioning

confidence: 99%

Inhibition of Nitric Oxide: Effects on Interleukin-lβ-Enhanced Ovulation Rate, Steroid Hormones, and Ovarian Leukocyte Distribution at Ovulation in the Rat1

Bonello

McKie

Jasper

et al. 1996

Biology of Reproduction

162

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“…Progesterone may act on the hypothalamic-pituitary pathway (Martin et al, 1983), or at the level of the ovary (Hunter et al, 1986;Brown et al, 1988) or uterus. This latter suggestion has been widely studied (Vallet et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Role of the uterus in early regression of corpora lutea induced by the ram effect in seasonally anoestrous Barbarine ewes

Lassoued¹,

Khaldi²,

Chemineau³

et al. 1997

Reprod. Nutr. Dev.

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Summary -The involvement of the uterus in early regression of corpora lutea induced by the ram effect was studied in seasonally anoestrous Barbarine ewes. In experiment 1, group I was only submitted to the male effect (control, n = 15) while group II (n = 14) was injected every 12 h with flunixin meglumine, a PGF2a synthetase inhibitor (finadyne), from day 3 to day 6 (day 0: day of ram introduction). The preovulatory LH surge appeared at the same time (around 21 h after ram introduction) in both groups. Finadyne treatment significantly decreased 13-14-dihydro-15-keto-PGF2a (PGFM) pulses ( 1.3 ± 0.3 versus 0.4 ± 0.2; P < 0.05), the number of short cycles (50 versus 14%, P < 0.05), and provided a single peak of oestrus, 15-16 days after the introduction of the rams, instead of between day 14 and day 23 (P < 0.01 In experiment 2, 17 hysterectomized ewes were allocated into two groups: group III (n = 8) was injected with oil and group IV (n = 9) received an intramuscular injection of 20 mg of progesterone immediately before introduction of rams. An additional group of intact ewes was used as control (group V, n = 9). Hysterectomy did not affect the ovulation response to the ram effect, but completely suppressed short cycles (0 versus 78% , P < 0.001). The preovulatory LH surge was delayed in hysterectomized females (36.0 ± 14.1 versus 16.6 ± 11.4 h; P < 0.004). Treatment with progesterone significantly (P < 0.01) increased the interval between introduction of rams and the preovulatory LH surge. In conclusion, suppression of short cycles by hysterectomy and an inhibitor of PGF2a synthetase suggest that the uterus is essential for determining the lifespan of ram-induced corpora lutea and that premature release of PGF2a is the cause of early luteal regression. The hypothesis that lower secretion of progesterone before D5 could be the initial cause of the premature induction of the luteolytic signal is discussed.

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Neuropeptide Y reduces ovarian blood flow in the rabbit

Jørgensen¹,

Sejrsen²

1990

Peptides

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Ovarian capillary blood flow in seasonally anoestrous ewes induced to ovulate by treatment with GnRH

Cited by 5 publications

References 4 publications

Inhibition of Nitric Oxide: Effects on Interleukin-lβ-Enhanced Ovulation Rate, Steroid Hormones, and Ovarian Leukocyte Distribution at Ovulation in the Rat1

Inhibition of Nitric Oxide: Effects on Interleukin-lβ-Enhanced Ovulation Rate, Steroid Hormones, and Ovarian Leukocyte Distribution at Ovulation in the Rat1

Role of the uterus in early regression of corpora lutea induced by the ram effect in seasonally anoestrous Barbarine ewes

Neuropeptide Y reduces ovarian blood flow in the rabbit

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