消炎痛及PGF_(2α)对在体培养人子宫内膜出血的影响

利用甾体激素撤退方法造成移植在地鼠颊囊内人子宫内膜出血的动物模型,研究消炎痛和PGF_(2a)对内膜出血的作用。结果表明,注射三种不同剂量消炎痛并不能完全抑制内膜出血,但对内膜出血时间有延缓作用。用两种不同剂量的PGF_(2a)采取缓慢释放给药方法,虽然地鼠在给药后外周血液中PGF_(2a)水平比给药前显著增高,但内膜出血并不出现在撤退甾体激素之前。结果提示,PGF_(2a)对内膜血管破裂无直接作用,而纤溶活性变化可能是触子宫内膜出血更直接的原因。     

首次报道甾体浓度和卵泡体积呈相反关系

以前曾报道,卵泡内甾体浓度和卵泡体积呈正比关系,但这些实验所测定的卵泡是来自周期不清的动物体;或来自经克罗米芬或hCG等处理的病人。H.J.M.Goverde等采用未经任何处理的,排卵前10h的金黄田鼠的卵泡,以测定卵泡中甾体的浓度,得出了完全相反的结果。卵泡液的收集是在LH峰和FSH峰开始时,卵泡数量为36个,卵泡体积(V;mm~(?)):0.0090.025的卵泡,E_2和P的平均浓度分别约为30.1和517;0.015相似文献   

不同剂量的抗孕-53和18-甲基炔诺酮对大鼠垂体机能反应性影响的比较

为了研究甾体避孕药对垂体生殖激素的影响,本实验以动情前期大鼠受二次静脉注射GnRH诱发的LH激发效应(priming effect)为模型,观察经肌肉注射不同类型、不同剂量的避孕药(抗孕-53或18-甲基炔诺酮)后垂体对GnRH的敏感性反应。抗孕-53的剂量为3,1.5,0.75,0.375和0.19mg;l8-甲基炔诺酮的剂量为4,1和0.5mg,各溶于0.5ml茶油;对照组为0.5ml茶油。实验结果表明,不同剂量的抗孕-53均促进血浆LH浓度升高,其中以3mg组的反应最显著,与对照组比较P<0.01。不同剂量的18-甲基炔诺酮对垂体敏感性均有显著的抑制作用,使血浆LH浓度降低(P<0.01)。大鼠经肌肉注射乙炔雌二醇21μg和10.5μg后,其垂体对GnRH的反应也有促进作用,但不能完全模拟抗孕-53的效应。上述结果表明,不同类型的甾体避孕药能增加或降低大鼠垂体对GnRH的敏感性。     

性腺素:卵泡液中刺激垂体促性腺激素分泌的肽

作者给22天的未成年雌性大鼠注射孕马血清促性腺激素,于25天处死,取卵巢,将卵泡液处理后得到大鼠卵泡液性腺素(gonadocrinin)的粗制剂。将此性腺素制剂加入垂体细胞单层培养以后,培养液中的LH和FSH均增加。而以同样方式处理大鼠肝脏所得到的制剂无此作用。在大鼠间情期第二天,静脉注射该性腺素,血清LH水平的变化与用LRF处理的大鼠相似。这说明,在体及离体条件下,性腺素均能刺激垂体分泌促性腺激素。离体条件下,性腺素仅仅刺激LH和FSH的分泌,对其它几种垂体激素(PRL、GH及TSH)的分泌均无影响。这提示性腺素的作用具有特异性。用放射免疫测定法证明,该性腺素制剂中没有可测出量的FSH、LH、雌激素、孕酮及睾丸酮。     

处理方式不同的颗粒细胞和卵泡液对牛卵母细胞体外受精后卵裂率和囊胚率的影响

将牛的卵母细胞置于添加有不同预处理颗粒细胞及含有卵泡液的培养液或不舍有卵泡液的培养液中进行体外成熟、受精及胚胎发育培养,研究了颗粒细胞、卵泡液及颗粒细胞与卵泡液交互作用对牛卵母细胞成熟、受精后卵裂率、囊胚率的影响。2178枚卵母细胞体外成熟受精后胚胎发育的对比观察结果表明：颗粒细胞、卵泡液及颗粒细胞与卵泡液交互作用对卵母细胞成熟受精后胚胎的卵裂具有显著影响（P〈0．05）;颗粒细胞对囊胚的发育有显著影响（P〈0．05）;卵泡液及颗粒细胞与卵泡液交互作用对囊胚的发育无显著影响（P〉0．05）。不同因素对卵裂率、囊胚率的影响表现为：颗粒细胞因素〉培养液因素〉培养液&#215;颗粒细胞交互作用。结论：TCM199培养液中添加卵泡液和单层颗粒细胞组成的培养系统用于牛卵母细胞体外成熟及胚胎发育的效果较好。共培养体系中的单层颗粒细胞用经酶消化分散处理后在培养箱中孵育10min的颗粒细胞替代时,胚胎的发育效果并不受影响。     

正常月经周期妇女卵泡液中激素水平的变化

本文测定了24例正常月经妇女在不同时相、不同大小卵泡的卵泡液中雌二醇(E_2)、孕酮(P_0)、雄烯二酮(A)、睾酮(T)、卵泡刺激素(FSH)、黄体生成素(LH)和催乳素(PRL)的含量,并分析其与外周血中相应激素浓度的关系。测定结果显示:小卵泡的卵泡液中E_2、Po,FSH,LH水平低于大卵泡中水平,而A和T水平则相反。排卵前大卵泡中E_2(9815nmol/L),P_0(3316nmol/L),FSH(1.34IU/L)和LH(3.9lIU/L)达最高值。A(280nmol/L)和T(137nmol/L)却较小卵泡中水平低(相应为692nmol/L和176nmol/L)。PRL水平在大小卵泡中无显著性差异。卵泡液中甾体激素水平高于外周血7—20.000倍,FSH、LH水平为外周血的10—80％,PRL水平为60％—3倍。     

十八反中藜芦与人参配伍化学成分变化的UPLC/Q-TOFMS研究

利用超高液相色谱串联飞行时间质谱（UPLC/Q-TOFMS）对中药十八反药对藜芦与人参配伍的合煎液与单煎后的合并液进行检测,经过MassLynx4.1软件分析,结果表明其化学成分存在差异,与人参配伍合煎后部分藜芦类甾体生物碱,如藜芦定碱、芥藜芦碱类、棋盘花胺类等的溶出增加,有可能致毒性增加;藜芦与人参配伍同时降低了人参皂苷类药效成分的含量,具有增毒减效的作用.     

甲氰咪胍能刺激降钙素释放

甲氰咪胍(cimetioine)是一种组织胺H_2受体拮抗剂,用于治疗胃液分泌过多。最近,一些实验提示,甲氰咪胍能抑制甲状旁腺激素(PTH)的分泌以及甲状旁腺组织中cAMP的产生。给正常人或病人用甲氰咪胍,能使血清中PTH的免疫反应降低。作者实验室进一步观察了甲氰咪胍是否也影响降钙素(CT)的释放。从幼年大鼠制备甲状腺-甲状旁腺复合体,在病人手术时得到甲状腺髓样癌组织,将适量组织放于Eagle氏液中,在37℃孵育。药物直接加入孵育液中。分别用特异的放射免疫分析法测定孵育液中的PTH和CT。结果发现,向大鼠的甲状腺-甲状旁腺复合体的孵育液中加入甲氰咪胍,PTH的分泌明显受抑制,而孵育液中的CT明显增加。甲氰咪胍也明显地刺激人甲状腺髓样癌组织释放CT。但是,组织胺或五肽胃素对人甲状腺髓样癌组织释放CT无任何影响。H_1受体阻断剂也不能刺激大鼠甲状腺C细胞释放CT。作者实验室首次报道了甲氰咪胍能直接作用于离体的大鼠和人的C细胞,刺激CT释放。当然,这种作用是否确实通过H_2受体以及其生理意义都有待阐明。     

卵泡液蛋白质组学2-DE体系的构建与应用

卵泡液是在卵泡形成过程中生成的,作为卵母细胞生长和分化的培养基,直接或间接影响卵母细胞的生育力和发育潜能,其成分非常复杂。本研究通过调整,优化2-DE技术条件,建立了相对稳定的卵泡液蛋白质2-DE技术,获得了卵泡液蛋白质组表达图谱,并用PDQuest软件进行了图像分析,用MALDI-TOF MS鉴定了9个蛋白点,其中有四种为新鉴定的在卵泡液中表达的蛋白质。结果表明,该体系稳定性、重复性好,为进一步开展卵泡液蛋白质组学的相关研究奠定了基础。     

不同水温下氟甲砜霉素在斑点叉尾鮰体内的药代动力学研究

研究不同水温(18℃和28℃)条件下,单剂量(10mg/kgb·w)强饲氟甲砜霉素,在斑点叉尾鮰(Ictaluruspunc-tatus)体内药代动力学特征.采用高效液相色谱紫外检测法可以同时检测血浆中氟甲砜霉素及其代谢物氟甲砜霉素的浓度.用3p97药代动力学软件处理药时数据.结果表明:在不同水温条件下氟甲砜霉素在斑点叉尾鮰体内的药时数据均符合一室开放式模型.药时规律符合理论方程C血浆=71921(e-0.036t-e-0.18t)和C血浆=91061(e-0.081t-e-0.301t).18℃和28℃的条件下,主要药代动力学参数:吸收半衰期T1/2ka分别为31845h和21301h,消除半衰期T1/2ke分别为191118h和81519h,达峰时间Tpeak分别为111136h和51953h,最大血药浓度Cmax分别为41074μg/mL和41226μg/mL,曲线下面积AUC分别为1741547(μg/mL)/h和811279(μg/mL)/h,平均驻留时间MRT分别为271581h和121290h,相对表观分布容积V/F(c)分别为11580L/kg和115121L/kg.采用氟甲砜霉素防治斑点叉尾鮰细菌性疾病,建议在18℃左右口服10mg/kg体重剂量的氟甲砜霉素,2d给药1次;在28℃左右口服10mg/kg体重剂量的氟甲砜霉素,1d给药1次.试验过程中在斑点叉尾鮰血浆样品中未检测到氟甲砜霉素的主要代谢物氟甲砜霉素胺.       

Ovarian steroidogenesis in Japanese patients with polycystic ovary syndrome

Gonadotropin and steroid hormone levels in both peripheral and ovarian venous blood were measured in samples obtained from 20 Japanese patients with polycystic ovary syndrome (PCOs) and 10 normal women in early follicular phase (normal women) by radioimmunoassay. The change in the amount of steroid hormone following intravenous human menopausal gonadotropin (HMG) or dexamethasone administration was investigated. The mean concentration in patients with PCOs was significantly higher than the concentrations found in normal women for LH (p less than 0.001), but not for FSH in peripheral blood. Significantly elevated ovarian venous steroid hormone levels in PCOs were found for 17 alpha-hydroxypregnenolone (p less than 0.05), progesterone (p less than 0.05), 17 alpha-hydroxyprogesterone (p less than 0.01), 4 delta-androstenedione (p less 0.01), testosterone (p less than 0.01), estrone (p less than 0.01) and estradiol (p less than 0.05), but not for dehydroepiandrosterone-sulfate (DHEAS). The ovarian dehydroepiandrosterone (DHEA) level was slightly elevated in PCOs. The concentration of ovarian 4 delta-androstenedione in PCOs reached twelve times as much as that in normal women. After the administration of HMG, all of the ovarian venus steroid hormone levels were elevated slightly and without significance in the short observation time for 10 min. The DHEAS level was suppressed while the ovarian DHEA level remained high in PCOs following dexamethasone administration. These findings seem to indicate there is no adrenal involvement and no adrenal-like component in the ovary of PCOs, and no evidence of 3 beta-hydroxysteroid dehydrogenase and/or aromatase deficiency in this study. The increase in the steroid hormone secretion in PCOs is explained by the increase in ovarian production in polycystic enlarged ovaries.     

孕马血清促性腺激素和氯地酚对猕猴超数排卵效果的观察

用孕马血清促性腺激素,总剂量为1550—2000单位,分4—7天处理猕猴,可促使其每侧卵巢出现滤泡超数发育,随后静脉注射入绒毛膜促性腺激素2500单位,在24小时内,猕猴即可出现超数排卵。     

The effects of orchidectomy and gonadotropins on steroidogenesis and oogenesis in Bidder's organs of the toad Bufo woodhousii.

In the family Bufonidae, male toads possess rudimentary ovaries, called Bidder's organs, which are attached to the testes. The mechanisms involved in the inhibition of oogenesis in these structures were investigated in male Bufo woodhousii. Orchidectomized and sham-operated animals were injected with gonadotropins (pregnant mare serum gonadotropin [PMSG] + human chorionic gonadotropin [hCG]) for 26 days and the effects of these hormones on oogenesis and steroidogenic activity (3 beta-hydroxysteroid dehydrogenase [3 beta-HSD] and 17 beta-HSD) in the Bidder's organ were quantified. Bilateral orchidectomy alone resulted in the growth of bidderian oocytes and a shift towards later stages of oogenesis. Gonadotropins enhanced this effect and stimulated the proliferation of new germ cells. In the presence of testes, however, bidderian oogenesis remained inhibited despite high levels of circulating gonadotropins. In both ooplasm and follicular layers of the bidderian oocytes of all toads, 3 beta-HSD and 17 beta-HSD activities were detected by histochemistry. Follicular enzymatic activity increased in orchidectomized toads treated with PMSG + hCG but decreased in sham-operated toads treated with gonadotropins. Testis weights, rudimentary oviduct weights, and plasma steroid levels increased in intact toads injected with hCG + PMSG. Gonadotropins had no effect on plasma steroid levels in orchidectomized toads, however. These results suggest that the testes play a major role in the inhibition of oogenesis in Bidder's organs of B. woodhousii and are a major source of androgens. High circulating levels of gonadotropins do not overcome the inhibitory effects of the testes.     

Ovarian contents of immunoreactive beta-endorphin and alpha-N-acetylated opioid peptides in rats

beta-Endorphin was measured by radioimmunoassay in homogenates of ovaries from immature Sprague-Dawley rats (21-29 days of age) and found to be present at levels of about 0.6-0.7 ng/ovary. After administration of PMSG there was approximately a 4-fold increase (2-3 ng/ovary) in total ovarian immunoreactive (ir) beta-endorphin 48 h after injection. Analysis of follicular fluid from similarly treated rats indicated about the same amount of ovarian ir-beta-endorphin (2-3 ng/ovary) as in ovarian homogenates, suggesting that most of the ir-beta-endorphin is localized in follicular fluid of PMSG-primed immature rats. Immature rats were made pseudopregnant by administration of hCG 48 h after PMSG, and at 24 h after injection of hCG there was a slight, but significant and reproducible, increase in the ovarian content of ir-beta-endorphin. The serum concentration of ir-beta-endorphin was in the range of 1-3 ng/ml and was unaffected by PMSG and PMSG/hCG; likewise, the pituitary content of ir-beta-endorphin did not change following administration of gonadotrophins to immature rats. In mature cyclic animals, levels of 2-4 ng ir-beta-endorphin/ovary were found, comparable to those in the ovaries of PMSG-primed immature rats, and there were only small changes during the oestrous cycle. In addition to ir-beta-endorphin, we also obtained evidence for the presence of alpha-N-acetylated opioid peptides (endorphins or enkephalins) in the ovaries of PMSG-primed immature and mature rats. The physiological role of the opioid peptides in reproductive tissue is unknown, but they are presumably acting in an autocrine or paracrine fashion.     

Steroid secretion rates and plasma binding activity in androstenedione-immune ewes with an autotransplanted ovary

Mature Merino ewes in which the left ovary and its vascular pedicle had been autotransplanted to the neck were divided into control (N = 5) and immunized groups (N = 6). The immunized ewes were treated (2 ml s.c.) with Fecundin 1 and 4 weeks before the start of blood sampling. Ovarian and jugular venous blood was collected every 10 min at two stages of the follicular phase (21-27 h and 38-42 h after i.m. injection of 125 micrograms of a prostaglandin (PG) analogue) and during the mid-luteal phase (8 h at 15-min intervals). The ewes were monitored regularly for luteal function and preovulatory LH surges. Hormone concentrations and anti-androstenedione titres were assayed by RIA and ovarian secretion rates of oestradiol-17 beta, progesterone and androstenedione were determined. After the booster immunization, progesterone increased simultaneously with titre in immunized ewes, reaching 30 ng/ml at the time of PG injection when median titre was 1:10,000. All ewes responded to PG with LH surges 42-72 h later: 2 of the immunized ewes then had a second LH surge within 3-4 days at a time when peripheral progesterone values were 2-3 ng/ml. The frequency of steroid and LH pulses was greater in immunized ewes (P less than 0.05) during the luteal phase but not the follicular phase. The secretion rate of androstenedione was 6-10 times greater (19-37 ng/min; P less than 0.001) in immunized ewes at all sampling stages. Progesterone secretion rates were 3 times greater (16 micrograms/min; P less than 0.001) during the luteal phase in immunized ewes. The amplitude of oestradiol pulses was significantly reduced in immunized ewes (4.8 vs 2.1 ng/min at +24 h and 6.5 vs 2.8 ng/min at +40 h in control and immunized ewes, respectively: P less than 0.05) during the follicular phase. However, the mean secretion rate of oestradiol at each phase of the cycle was not significantly different between treatment groups. Analysis of bound and free steroid using polyethylene glycol showed that greater than 98% of peripheral and ovarian venous androstenedione and 86% of peripheral progesterone was bound in immunized ewes but there was no appreciable binding (less than 0.1%) in control ewes. Similarly, 50% of ovarian venous oestradiol was bound in immunized ewes compared to 15% in control ewes. We conclude that immunization against androstenedione increases the secretion rate of androstenedione and progesterone but not of oestradiol.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of FGA and PMSG on follicular growth and LH secretion in Suffolk ewes

The effects of fluorogestone acetate (FGA) and/or pregnant mare serum gonadotrophin (PMSG) on follicular growth and LH secretion in cyclic ewes were determined. Suffolk ewes (n = 40), previously synchronized with cloprostenol were divided into 4 experimental groups (n = 10 ewes per group). Group I served as the control, while groups II, III and IV received FGA, PMSG, FGA and PMSG respectively. Four ewes of each group underwent daily laparascopy for 17 d. All the ovarian follicles >/= 2 mm were measured, and their relative locations were recorded on an ovarian map in order to follow the sequential development of each individual follicle. Comparisons were made of the mean day of emergence and the mean number of small, medium and large follicles, the atresia rate and the ovulation rate. For each group, 3 waves of follicular growth and atresia were observed during the cycle. During luteal phase, FGA treatment accelerated the mechanisms of follicular growth but reduced the number of large follicles and increased the atresia rate. In the follicular phase, FGA treatment was detrimental to both the number of large follicles and the ovulation rate. By contrast, PMSG enhanced recruitment of small follicles and the ovulation rate. Serial blood samples were collected during the luteal and follicular phases to study LH secretion. None of the treatments had any effect on LH secretion patterns.     

Ovarian activity in progesterone treated mares following administration of pregnant mare serum gonadotropin

Twelve non-pregnant, non-lactating mares were randomly assigned to four treatment groups using a 2x2 factorial arrangement with three replicates per group. Mares were administered PGF(2alpha) (10 mg, IM) on days -14 and 0, followed by HCG (3000 IU, IM) on day 5. The following treatments were administered: Group A received PMSG on days 2 (4000 IU, IM) and 5 (1000 IU, IV); Group B received PMSG (4000 IU, IM) on day 2; Group C received PMSG (1000 IU, IV) on day; Group D received no PMSG. Mares received progesterone (25 mg, IM) on days 1 through 4. Reproductive tracts were recovered at necropsy on day 16 (10 days post-ovulation). Ovaries were weighed, CL number and weight determined, follicles counted and measured, and volume of follicular fluid quantified. Mean ovarian weight (g) and number of CL per mare, respectively were: Group A, 100.0+/-15.6, 1.7+/-.7; Group B, 128.6+/-40.4, 1.3+/-.7; Group C, 92.4+/-21.0, 2.0+/-.0; Group D, 93.3+/-12.3; .3+/-.3. Mean number of follicles >10 mm and total volume (ml) of follicular fluid per mare, respectively, were: Group A, 9.4+/-2.0, 21.8+/-10.9; Group B, 1.3+/-.3, 32.2+/-28.9; Group C, 4.3+/-1.8, 5.4+/-2.3; Group D, 6.0+/-4.5, 24.0+/-10.3. There was no difference (P>.05) in mean ovarian weight, CL number, CL weight, follicular fluid volume, number of follicles, or size of follicles between treatment groups. These results show no significant effect on ovarian activity in progesterone treated mares following administration of exogenous PMSG.     

Direct effects of ovine follicular fluid on ovarian steroid secretion and expression of markers of cellular differentiation in sheep

The objective of this study was to assess the effect of ovine follicular fluid (FF) treatment (with or without FSH replacement) during the late follicular phase on plasma concentrations of gonadotrophins and the development of the ovulatory follicle. Ovarian steroid secretion and expression of mRNA encoding inhibin alpha and beta A, beta B subunits, P450 aromatase and P450 17 alpha-hydroxylase were used as endpoints. After induction of luteolysis by injection of 100 micrograms cloprostenol on days 10-12, Scottish Blackface ewes were allocated to one of three groups: (1) control (n = 7): no further treatment; (2) FF (n = 9): subcutaneous injections of 3 ml steroid-free ovine follicular fluid at 9 h intervals, 18 and 27 h after cloprostenol injection; (3) FF + FSH (n = 8): injections of follicular fluid as above plus subcutaneous injections of 0.36 iu ovine FSH at 6 h intervals, 18, 24, and 30 h after cloprostenol injection. Jugular venous blood samples were obtained via indwelling cannulae at 6 h intervals from 0 to 36 h after cloprostenol injection, and at 10 min intervals from 12 to 18 h (control phase) and from 30 to 36 h after cloprostenol injection (treatment phase). At laparotomy, 36 h after cloprostenol injection, ovarian venous blood was collected and ovaries were removed and processed for in situ hybridization. Plasma concentrations of FSH, luteinizing hormone (LH) and oestradiol were determined by radioimmunoassay. Follicular fluid treatment resulted in a decrease (P < 0.001) in FSH concentrations associated with an acute decrease in ovarian steroid secretion (P < 0.01) and a specific depression in P450 aromatase, (P < 0.001), inhibin-activin beta B subunit (P < 0.05) and thecal LH receptor (P < 0.001) expression. Follicular fluid treatment had no effect on inhibin-activin alpha and beta A, subunit or P450 17 alpha-hydroxylase expression. FSH co-treatment with follicular fluid restored circulating FSH concentrations to normal values and reversed some of the effects of follicular fluid (androstenedione, testosterone and progesterone secretion, and inhibin beta B and thecal LH receptor expression) but not oestradiol secretion or P450 aromatase expression. It was concluded that the actions of follicular fluid are mediated via both central effects on pituitary FSH secretion and by direct ovarian effects on granulosa cell aromatase activity. The results indicate that follicular fluid contains a factor that inhibits aromatase activity of granulosa cells directly and may play a role in the selection of the dominant follicle.     

Effects of monoclonal antibody against PMSG administered shortly after the preovulatory LH surge on time and number of ovulations in PMSG/PG-treated cows

Normally cyclic heifers received 2500 i.u. PMSG i.m. at Day 10 of the oestrous cycle and 15 mg prostaglandin (PG) i.m. 48 h later. From 30 h after PG the LH concentration in the peripheral blood was estimated every hour using a rapid RIA method which allowed the LH concentration to be known within 4 h. Monoclonal antibody against PMSG was injected in the jugular vein of 29 heifers at 4.8 h after the maximum of the preovulatory LH peak; 28 heifers were not treated with anti-PMSG (controls). Peripheral blood concentrations of PMSG, LH, progesterone and oestradiol were compared. Ovaries were collected by ovariectomy at fixed times, 22-30 h after the LH peak, and numbers were counted of small (2-10 mm), large (greater than 10 mm) and ovulated follicles, and of follicles with a stigma. In anti-PMSG-treated cows, the PMSG concentration fell sharply to non-detectable levels within 2 h of the treatment, indicating that PMSG was neutralized in these cows at the onset of final follicular maturation. In all cows, the concentration of oestradiol showed a significant decrease at about 8 h after the LH peak. After anti-PMSG treatment ovulations took place from 24 until 30 h after the LH peak, whereas in control cows follicles had already ovulated at or before 22 h and ovulations continued until 30 h. At 30 h 90% of the follicles had ovulated in anti-PMSG-treated cows vs 72% in the controls, resulting in 15 and 8 ovulations per cow respectively (P less than 0.05). Also, administration of monoclonal antibody against PMSG synchronized final follicular maturation and shortened the period of multiple ovulations. In conclusion, neutralization of PMSG shortly after the preovulatory LH peak suppresses adverse effects of PMSG on final follicular maturation, leading to an almost 2-fold increase of the ovulation rate.