Oocyte production and ovarian steroid concentrations of immature rats in response to some commercial gonadotrophin preparations

1990 ◽  
Vol 2 (6) ◽  
pp. 671 ◽  
Author(s):  
KM Henderson ◽  
A Weaver ◽  
RL Wards ◽  
K Ball ◽  
S Lun ◽  
...  

Four commercial gonadotrophin preparations, namely Folligon, F.S.H.-P., Folltropin and Ovagen, were examined for their effects on oocyte production and ovarian steroid concentrations in immature rats. The ratios of the FSH to LH concentrations of the preparations, determined by radioreceptor assays, were Folligon 5, F.S.H.-P. 18, Folltropin 49 and Ovagen 1090. Forty-eight hours after administering each gonadotrophin preparation to immature rats, ovulation was induced by injection of chorionic gonadotrophin. Twenty-four hours later, oocytes were recovered from the oviducts and counted. Oocytes were produced after injection of chorionic gonadotrophin following a single injection of Folligon (10-50 i.u.). However, no oocytes were produced in response to the other gonadotrophin preparations unless they were administered by continuous infusion (30-1000 micrograms day-1). When given by injection (Folligon) or infusion (others), the gonadotrophin preparations all promoted a dose-dependent increase in mean oocyte production, except at the highest doses when mean oocyte numbers either remained unchanged or declined significantly in the cases of Folligon and F.S.H.-P. The highest mean numbers of oocytes produced in response to Folltropin (48 +/- 9 oocytes, mean +/- s.e.m.) and Ovagen (47 +/- 7) were greater than those attained with Folligon (21 +/- 6) or F.S.H.-P. (31 +/- 5). Mean ovarian weights also increased in a dose-dependent fashion in response to each of the gonadotrophin preparations. Measurements of ovarian steroid concentrations 48 h after the onset of gonadotrophin treatment (i.e. immediately prior to ovulation induction with chorionic gonadotrophin) showed that the gonadotrophin preparations markedly influenced the ratios of ovarian oestradiol-17 beta and androgen (androstenedione plus testosterone) concentrations. At low doses the gonadotrophin preparations increased the ratio of oestradiol-17 beta to androgens, but at the highest doses, with the exception of Ovagen, the ratio was reduced relative to peak values. Co-infusion of ovine LH (NIADDK-oLH-25; 10-20 micrograms day-1) with Ovagen (250 micrograms day-1) or ovine FSH (10 micrograms day-1, NIADDK-oFSH-17), both low in LH content, increased the mean number of oocytes produced and also the ovarian oestradiol-17 beta:androgen concentration ratio. However, with 40 micrograms LH day-1, the oestradiol-17 beta:androgen ratio fell due to a continued increase in mean ovarian androgen concentrations and a decrease in mean ovarian oestradiol-17 beta concentration. The mean number of oocytes produced also fell significantly.(ABSTRACT TRUNCATED AT 400 WORDS)

1980 ◽  
Vol 84 (3) ◽  
pp. 333-341 ◽  
Author(s):  
TAKAHIDE MORI ◽  
HEIGO KOHDA ◽  
YASUSHI KINOSHITA ◽  
YOJIRO EZAKI ◽  
NORIHIKO MORIMOTO ◽  
...  

Treatment of immature rats with pregnant mare serum gonadotrophin followed by human chorionic gonadotrophin (HCG) caused an acute and temporary increase in concentrations of progesterone, testosterone and oestradiol in plasma with maximum levels 3 h after the administration of HCG. Concurrent injection of indomethacin and HCG reduced, in a dose-dependent manner, the mean number of ova shed and this was accompanied by a dose-dependent decrease in concentrations of plasma progesterone and testosterone but not of oestradiol when they were measured 3 h after the injection of HCG. The minimum effective dose that blocked ovulation completely at 0 h abolished the acute increase of progesterone and testosterone, suggesting that prostaglandins act on ovulation by stimulating steroidogenesis at an early stage in the preovulatory process. The anti-ovulatory action of the minimum effective dose at 0 h became progressively less potent as the time between injection of HCG and administration of indomethacin was increased, although plasma concentrations of progesterone and testosterone measured at autopsy 18 h after treatment with HCG had not changed appreciably. When indomethacin was administered 10 h after HCG, the relationship between the dose of indomethacin and the mean number of ova differed from that observed when simultaneous injections of indomethacin and HCG were given, and the minimum effective dose that prevented ovulation was much higher than that at 0 h, suggesting that prostaglandins act differently on ovulation in the later stage of the preovulatory process. It was concluded that prostaglandins may mediate the action of HCG on ovulation through two mechanisms which operate at different stages of the preovulatory process.


1989 ◽  
Vol 256 (6) ◽  
pp. H1747-H1751 ◽  
Author(s):  
Y. Ouchi ◽  
S. Kim ◽  
A. C. Souza ◽  
S. Iijima ◽  
A. Hattori ◽  
...  

This study was conducted to investigate the effect of intracerebroventricular administration of endothelin (EDT), a novel potent vasoconstricting peptide, on blood pressure in conscious rats. The lateral cerebral ventricle of male Wistar rats was cannulated, and the femoral artery was also cannulated to measure the mean arterial blood pressure (MABP) and heart rate (HR). EDT dissolved in 10 microliters of artificial cerebrospinal fluid (ACSF) (8.25-66 pmol icv) provoked a dose-dependent increase in MABP. EDT also increased HR, although the effect of 66 pmol was variable. Intracerebroventricular ACSF did not provoke any effects on MABP and HR. Intracerebroventricular EDT also provoked contralateral rotational behavior. Pretreatment with 2 mg/kg iv phenoxybenzamine significantly suppressed the 16.5 pmol icv EDT-induced increase in MABP. Moreover, 16.5 pmol icv EDT markedly increased plasma epinephrine and norepinephrine concentration. These results indicate that EDT has a central pressor action, and the action might be mediated, at least in part, by catecholamine release to the periphery. EDT might play a role in the central control of blood pressure, although the physiological implications have not yet been determined.


2020 ◽  
Vol 21 (15) ◽  
pp. 5385
Author(s):  
Christiaan M. Suttorp ◽  
René E. M. van Rheden ◽  
Natasja W. M. van Dijk ◽  
Maria P. A. C. Helmich ◽  
Anne Marie Kuijpers-Jagtman ◽  
...  

Both infectious as non-infectious inflammation can cause placental dysfunction and pregnancy complications. During the first trimester of human gestation, when palatogenesis takes place, intrauterine hematoma and hemorrhage are common phenomena, causing the release of large amounts of heme, a well-known alarmin. We postulated that exposure of pregnant mice to heme during palatogenesis would initiate oxidative and inflammatory stress, leading to pathological pregnancy, increasing the incidence of palatal clefting and abortion. Both heme oxygenase isoforms (HO-1 and HO-2) break down heme, thereby generating anti-oxidative and -inflammatory products. HO may thus counteract these heme-induced injurious stresses. To test this hypothesis, we administered heme to pregnant CD1 outbred mice at Day E12 by intraperitoneal injection in increasing doses: 30, 75 or 150 μmol/kg body weight (30H, 75H or 150H) in the presence or absence of HO-activity inhibitor SnMP from Day E11. Exposure to heme resulted in a dose-dependent increase in abortion. At 75H half of the fetuses where resorbed, while at 150H all fetuses were aborted. HO-activity protected against heme-induced abortion since inhibition of HO-activity aggravated heme-induced detrimental effects. The fetuses surviving heme administration demonstrated normal palatal fusion. Immunostainings at Day E16 demonstrated higher numbers of ICAM-1 positive blood vessels, macrophages and HO-1 positive cells in placenta after administration of 75H or SnMP + 30H. Summarizing, heme acts as an endogenous “alarmin” during pregnancy in a dose-dependent fashion, while HO-activity protects against heme-induced placental vascular inflammation and abortion.


1981 ◽  
Vol 98 (3) ◽  
pp. 321-325 ◽  
Author(s):  
Anna C. Tate ◽  
A. D. Swift

Abstract. Extract of hypothalami was prepared which contained peptidase capable of degrading LRH. The degradation of LRH by this extract either alone or under the influence of oestrogens, androgens and cholesterol, when added to the extract was measured. Oestrone, oestradiol and oestriol (1 pg to 100 pg) stimulated mean peptidase activity significantly (P< 0.001) in a dose-dependent manner. Testosterone (0.1 ng to 10 ng) also caused a dose-dependent increase in degradation of LRH, the two highest doses used significantly increasing the mean activity (P < 0.001). Only the highest dose of androstenedione (10 ng) or dehydroepiandrosterone (10 ng) caused a significant increase of the mean LRH degradation (P < 0.05). Neither cholesterol nor dihydrotestosterone increased peptidase activity when added to the extract. It is suggested that it is possible that these peptidase enzymes could occupy a role in the negative feedback of steroids on the hypothalamus.


1986 ◽  
Vol 251 (2) ◽  
pp. R258-R263
Author(s):  
J. C. Lee ◽  
D. M. Denbow ◽  
M. D. Ashen ◽  
A. D. Roudabush

The purpose of this investigation was to examine the possible involvement of the central renin-angiotensin system in the pressor response to the intracerebroventricular (icv) injection of hypertonic NaCl in conscious turkeys. The icv injection was accomplished via a stereotaxically implanted stainless steel guide cannula in the lateral cerebral ventricle. The arterial blood pressure (AP) of the turkey was measured by means of a PE catheter in the left brachial artery. The icv administration of hypertonic NaCl caused a dose-dependent increase of AP. The mean AP increases due to 10-microliter icv injections of 0.9, 3.6, and 7.2% NaCl were 1.4 +/- 1.4, 18.1 +/- 3.0, and 31.2 +/- 3.2 (SE) mmHg, respectively. These changes were statistically significant (P less than 0.001). The icv administration of captopril, [Sar1, Ile8]angiotensin II, or pentobarbital sodium markedly reduced the pressor response to the icv injection of hypertonic 7.2% NaCl. Blockade of central adrenergic receptors with phentolamine and propranolol was without effect. These results support the contention that the central renin-angiotensin system may directly contribute to pressor responses induced by central hypertonic NaCl stimulation.


1983 ◽  
Vol 245 (5) ◽  
pp. G651-G655 ◽  
Author(s):  
J. Reichen ◽  
M. Le

To determine whether bile salts alter the permeability of the biliary tree to inert solutes, we investigated the effects of taurocholate and taurodehydrocholate on [14C]sucrose bile-to-plasma ratio in the situ perfused rat liver. Sucrose bile-to-plasma ratio remained virtually constant over a 3-h period in untreated rats. Infusing increasing amounts of taurocholate produced the anticipated dose-dependent increase in bile flow and bile salt secretion up to a maximal secretory rate of 278 nmol X min-1 X g liver-1. When the secretory rate was exceeded, bile flow decreased by 22%. Even at doses below the maximal secretory rate, sucrose bile-to-plasma ratio increased in a dose-dependent fashion. To determine whether this was due to recruitment of more permeable centrizonal hepatocytes, the effect of equimolar amounts of taurodehydrocholate was determined. This nonmicelle-forming bile salt led to more marked choleresis than taurocholate but did not affect sucrose bile-to-plasma ratio. We conclude that taurocholate, but not taurodehydrocholate, leads to a dose-dependent increase in biliary permeability.


1981 ◽  
Vol 48 (1) ◽  
pp. 181-191
Author(s):  
A.M. Rich ◽  
S.T. Hoffstein

The random migration of neutrophils under agarose as measured by the number of cells leaving the well, is enhanced when the pH or the osmolality of the medium is reduced or when microtubule agents are used. Concentrations of colchicine above 5 × 10-7 M increased the number of cells migrating and decreased the mean number of centriolar microtubules in a dose-dependent fashion from 16 to 4 per 4 micron 2 at 10-5 M. The distance that colchicine-treated neutrophils migrated from the well was not different from the control. Lowering the pH from 7.4 to 6.0 also increased random migration and decreased pericentriolar microtubules from a mean of 16 to a mean of 10. At pH 6.0, both the number of cells that migrated and the distance the cells forming the leading edge travelled from the well were increased. Since peripheral microtubules may play a greater role in cell migration than centiolar ones, we examined the numerical density of microtubules in the peripheral cytoplasm. Lowering the medium pH reduced the mean number of microtubules per 10 micron 2 from 6 to 2. Colchicine reduced micro-tubules in the same area to I. At the low pH, colchicine reduced even further the numbers of both centriole-associated and peripheral microtubules but the migration pattern was the same as that seen at pH 6.0 without colchicine. Lowering medium osmolality from 280 to 230 m-osmol increased random migration but did not affect microtubule numbers. The addition of colchicine to this system decreased microtubule numbers and increased migration even further. Conditions that enhanced neutrophil migration also affected cell shape. Whereas cells at pH 7.4 were generally fan-shaped with a broad, smooth leading edge, cells at pH 6.0 with or without colchicine were long and narrow. Neutrophils at pH 7.4 but 230 m-osmol had a scalloped edge, which often appeared thickened. This too was not altered by colchicine. The morphology of cells treated with colchicine was similar to controls except for the more frequent presence of long retraction fibres. Each of these treatments thus appears to act on a different aspect of the cell's locomotory apparatus. The mechanisms by which colchicine and lowered ph enhance migration may partially overlap since both significantly decrease peripheral microtubules. The data suggest that microtubules play a constraining role within the cell, limiting the ability of the cell to move and change direction.


2000 ◽  
Vol 167 (3) ◽  
pp. 465-471 ◽  
Author(s):  
J Bonser ◽  
J Walker ◽  
A Purohit ◽  
MJ Reed ◽  
BV Potter ◽  
...  

Dehydroepiandrosterone sulphate (DHEAS) is the most abundant androgen in the circulation and in ovarian follicular fluid. A steroid sulphatase accepting DHEAS as a substrate has been identified in the follicle, but the cellular location has not been determined. As DHEAS is also a potential source of oestrogen for endocrine-dependent tumours, a potent steroid sulphatase inhibitor oestrone-3-O-sulphamate (EMATE) has been developed which inhibits this activity in rat liver and mammary tumour. The aim of this study was to investigate human granulosa cells as a site of steroid sulphatase activity, to determine whether DHEAS can be utilized as a precursor for oestrogen synthesis and to investigate the inhibitory capacity of EMATE in these cells. Conversion of DHEAS to DHEA was assessed in luteinized granulosa cells by tritiated steroid assay following incubation with or without LH or insulin and steroid accumulation in the medium measured by RIA. The effects of EMATE were assessed by addition of a range of doses during the measurement of conversion of DHEAS to DHEA. Cells from three sizes of small follicles from an unstimulated ovary were also assessed for their ability to produce oestradiol from DHEAS. Sulphatase enzyme activity was present in all cells; the mean conversion of tritiated DHEAS to DHEA was 50% (range 4-65%). LH and EMATE inhibited and insulin stimulated this activity. Addition of DHEAS to granulosa cells caused a dose-dependent increase in oestradiol and androstenedione production with no change in progesterone concentration. LH increased the accumulation of oestradiol in the medium. DHEAS also stimulated oestradiol production by granulosa cells from small follicles. This is the first demonstration that granulosa cells are a site of sulphatase activity and that DHEAS can be utilized as a substrate for androstenedione and oestrogen production. This may be of physiological importance for both normal folliculogenesis and oestrogen-dependent tumour growth.


1971 ◽  
Vol 49 (4) ◽  
pp. 581-589
Author(s):  
R. H. F. HUNTER

SUMMARY Capacitation and fertilization during pseudopregnancy in the rabbit were examined on Days 4, 6, 8, 10 and 12 after mating with vasectomized males. At each of these five stages of pseudopregnancy, ovulation was induced in ten animals by a single injection of human chorionic gonadotrophin (HCG); an additional group of oestrous rabbits was similarly injected to serve as controls. Ejaculated spermatozoa were inseminated directly into the Fallopian tubes during laparotomy performed 2 h after the ovulating injection, and 15–22 h later the eggs were examined microscopically for evidence of fertilization. The mean number and range of induced ovulations decreased between Days 4 and 12 of pseudopregnancy. An overall recovery of 66% of the eggs resulting from these ovulations was achieved, the great majority being located in the Fallopian tubes. Fertilized eggs were obtained from 93% of the 60 does and 84% of the recovered eggs were fertilized. There was neither a decrease in the level of fertilization with advancing stages of pseudopregnancy, nor did the stage of pseudopregnancy influence the rate of development from pronuclear to four-celled eggs. Conspicuous among the small number of abnormal fertilizations were four dispermic pronuclear eggs and two digynic pronuclear eggs. It is concluded that after injection of HCG, complete capacitation of ejaculated spermatozoa can be achieved in the Fallopian tube between Days 4 and 12 of pseudopregnancy as rapidly as in the tube of oestrous rabbits. Furthermore, a high proportion of the eggs induced to ovulate during pseudopregnancy can be fertilized, though their potential for full embryonic development requires further study.


2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Yosouf Mohsenzadeh ◽  
Asghar Rahmani ◽  
Javad Cheraghi ◽  
Maryam Pyrani ◽  
Khairollah Asadollahi

This study aimed to investigate any inflammatory effect of nicotine on rat embryo by exposing their mothers to different dosages of nicotine during pregnancy. During this experimental study, 32 pregnant healthy Wistar rats were divided into 4 equal groups, including a control and 3 nicotine exposure groups. Injections were performed subcutaneously starting at the first day of pregnancy until parturition. As the dosages of nicotine were increased, the weight gain by pregnant rats and the mean weight of their newborns were significantly reduced. Mean ± SD of hs-CRP was significantly higher among groups exposed to various dosages of nicotine (2, 4, and 6 mg/kg) compared to the control group (P<0.0001) and its increasing rate was also dose dependent. Mean ± SD serum level of IL-6 and TNF-αamong all groups exposed to nicotine, except for 2 mg/kg nicotine injected group, was increased significantly (P<0.0001). Mean ± SD of serum level of TGF-βand nitrite oxide among exposure groups showed significant differences compared to the control group only at the dosage of 6 mg/kg (P<0.0001). The current study showed that exposing pregnant rats to nicotine causes a dose dependent increase in the rate of all the studied inflammatory serum markers among their newborns.


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