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Biomedical subjects

M P Walker

Publications and source records attributed to M P Walker.

At least 37 records · Page 2Linked to original sources

Indomethacin and arginine vasopressin interaction in the fetal kidney: a mechanism of oliguria.

OBJECTIVE: Indomethacin has been shown to cause fetal oliguria in humans and animals. This study was designed to test the hypothesis that indomethacin-induced fetal oliguria is mediated through the renal action of arginine vasopressin. STUDY DESIGN: Twenty-seven late-gestation (129 +/- 4 days [mean +/- SE]) chronically catheterized fetal sheep were studied. After a 1-hour control period fetal responses to indomethacin, 0.05 mg/kg given intravenously, followed by a 4-hour maintenance infusion (n = 9), were compared with an identical indomethacin infusion plus an arginine vasopressin V2-receptor antagonist (d[CH2]1(5), D-Phe2, Ile4,Arg8,Ala9)-VP (n = 8) or vehicle alone (n = 10). Fetal arterial and venous pressures, heart rate, and urinary flow were measured continuously. RESULTS: Fetal urinary flow rate (p < 0.0001) and free water clearance (p = 0.004) fell in response to indomethacin alone, but the addition of the arginine vasopressin V2-receptor antagonist blocked indomethacin's oliguric and free water effect. Urinary osmolality and sodium increased in both indomethacin and indomethacin+arginine vasopressin V2-receptor antagonist groups compared with vehicle (p < 0.05). Fetal arterial pressure increased in response to indomethacin, and the addition of the arginine vasopressin V2-receptor antagonist potentiated this response (p = 0.007). CONCLUSIONS: These results suggest that (1) fetal oliguria secondary to indomethacin is mediated through the stimulation of the renal arginine vasopressin V2-receptor and (2) prostaglandin synthesis inhibition may play a role in renal tubular sodium handling. In addition, the arginine vasopressin V2-receptor plays a role in ameliorating the hypertensive response to indomethacin. We speculate that indomethacin stimulates circulating arginine vasopressin levels and enhances peripheral arginine vasopressin effects in the fetus, resulting in oliguria and hypertension.

Animals↗

Detection of a kallikrein in the mouse lactating mammary gland: a possible processing enzyme for the epidermal growth factor precursor.

Kallikreins are a multigene subfamily of serine proteases that may have a role in processing precursors of polypeptide hormones and growth factors. The epidermal growth factor (EGF) immunoreactivity in mouse milk is derived from the membrane-bound EGF precursor located on the lumenal border of the alveolar cells in the mammary gland. Release of EGF into the milk requires the hydrolysis of the EGF precursor at Arg-X cleavage sites. We report the presence of a candidate EGF precursor-processing enzyme in the lactating mouse mammary gland. Kallikrein transcripts in the mouse lactating mammary gland were detected by primer-directed enzyme amplification of complementary DNA (cDNA). Primers to selected conserved regions of the kallikrein cDNA resulted in an amplified product of the predicted size (573 basepairs). Sequence analysis of the product over three nonconserved regions identified mGK-6 (mouse renal kallikrein) as the primary kallikrein in BALB/c mouse lactating mammary gland. Transcription products for the EGF-binding protein (mGK-9), mGK-1, MGK-3, and mGK-4 were not detected by enzyme amplification with specific primers corresponding to these kallikrein cDNAs. Positive immunohistochemical staining of the apical membrane of mammary alveolar cells was detected with a polyclonal antiserum to mouse kallikrein. Incubation of cell membranes isolated from lactating mammary glands released soluble EGF-immunoreactive material. Aprotinin partially inhibited the release of this material, whereas other protease inhibitors, such as leupeptin, benzamidine, and limabean trypsin inhibitor, had no detectable effect. These results support the hypothesis that the release of EGF-immunoreactive material into the milk is in part dependent upon a kallikrein enzyme (mGK-6) in the BALB/c mouse lactating mammary gland.

Animals↗

Expression of epidermal growth factor in suprabasal cells of stratified squamous epithelia: implications for a role in differentiation.

There is a disparity in the fact that epidermal growth factor (EGF) can stimulate proliferation of a wide variety of cells in vitro, yet sites of synthesis for this polypeptide in vivo are generally associated with nonproliferative or differentiated cell populations. Unlike other known mitogenic members of the EGF family of ligands, EGF derives from a large (M(r) approximately 130,000) protein that contains multiple EGF-like domains; some of these domains contain putative Ca(2+)-binding sites. In the present study, the mouse vaginal epithelium was used as a prototype tissue to investigate expression of the EGF precursor by stratified squamous epithelia. Stratification and cornification in this tissue are estrogen dependent. In the fully differentiated epithelium, EGF precursor transcripts were detected by in situ hybridization in suprabasal cells; labeling was not observed in the proliferative basal cell compartment. Amplified transcripts of predicted size were detected in the vaginal organ by the reverse transcription-polymerase chain reaction and Northern hybridization of polyadenylated RNA. Antisera to mature EGF or to the COOH-terminal (cytoplasmic) domain of the precursor localized reactivity exclusively to cells of the granular layer. The staining with the precursor antiserum was localized along cell borders, which supports that this protein is translocated to the cell membrane following synthesis, a known property for precursors of EGF-like ligands. EGF expression was not apparent in the atrophic vaginal epithelium of castrates, which did not present a granular layer. Other stratified squamous epithelia in organs such as skin, esophagus, and tongue also revealed EGF/EGF precursor immunoreactivity in the granular layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Indomethacin-induced urinary flow rate reduction in the ovine fetus is associated with reduced free water clearance and elevated plasma arginine vasopressin levels.

OBJECTIVE: The purpose of our study was to explore the urinary responses of the ovine fetus to indomethacin levels comparable with those used therapeutically in the human fetus. STUDY DESIGN: After a 1-hour control period, chronically catheterized ovine fetuses between 125 and 139 days of gestation were given an intravenous bolus of indomethacin (0.05 mg/kg estimated fetal weight) followed by a 0.0025 mg/kg/min continuous infusion for 5 hours. The experimental group (n = 9) was compared with a vehicle-only infusion group (n = 10). RESULTS: There was a sustained 55.7% +/- 9.5% (mean +/- SEM) decrease in urinary output by 2 hours of indomethacin infusion (p < 0.00001, analysis of variance). Urinary osmolality, potassium, and chloride concentrations underwent sustained increases during the infusion period (p < 0.005). Free water clearance decreased by 67.5% +/- 12.0% (p < 0.001). Fetal arterial pressure increased only transiently (p < 0.05), and increases in venous pressure (p = 0.013) and heart rate (p < 0.0001) were sustained. Fetal plasma arginine vasopressin concentration increased during indomethacin infusion (p < 0.05) and was correlated with the fall in urinary flow rate and free water clearance (p = 0.002). During vehicle infusion no significant changes were observed in any of the variables. CONCLUSIONS: Our data indicate that the fetus undergoes antidiuresis when exposed to low levels of indomethacin and that the observed antidiuresis is mediated by a decrease in free water clearance. The reduction in free water clearance may be mediated by increases in plasma arginine vasopressin concentrations.

Animals↗

Urinary and cardiovascular responses to indomethacin infusion in the ovine fetus.

OBJECTIVE: Our objective was to explore the urinary and cardiovascular responses of the near-term ovine fetus to plasma indomethacin levels similar to those in the human neonate undergoing indomethacin therapy. STUDY DESIGN: Chronically catheterized ovine fetuses between 125 and 139 days of gestation were studied. After a 1-hour control period we gave a bolus of 0.35 mg/kg estimated fetal weight of indomethacin into a fetal vein, followed by a 0.017 mg/kg/min continuous infusion for 5 hours (n = 9). Results were compared with a vehicle-infusion-only group (n = 10). RESULTS: During the first 3 hours of indomethacin infusion, fetal urinary output was increased by an average of 84.9% +/- 55.6% (analysis of variance, p less than 0.01). Urinary osmolality and sodium and chloride concentrations underwent sustained increases throughout the infusion period (p less than 0.001). Sodium excretion increased by 212% +/- 111% (p less than 0.05). Fetal arterial and venous pressures increased (p less than 0.001), and the change in urinary flow correlated positively with the change in arterial pressure (R = 0.55, p = 0.014). Fetal heart rate increased by 10% +/- 4% 1 hour after the bolus and remained elevated throughout the remainder of the infusion relative to vehicle-infused animals (p less than 0.001). Vehicle infusion had no effect on any fetal variable. CONCLUSIONS: This study does not support the hypothesis that indomethacin acutely reduces urinary flow rate in the late-gestation ovine fetus. Further, the observed urinary flow increases may be mediated in part by a pressure diuresis.

Animals↗

32P-postlabeling analysis of the formation and persistence of DNA adducts in mammary glands of parous and nulliparous mice treated with benzo[a]pyrene.

The susceptibility of the rodent mammary gland to known chemical carcinogens can vary with the stage of gland development. Full-term pregnancy (parity) can confer permanent structural and functional changes in the gland that are associated with decreased breast cancer risk in humans and protection from mammary carcinogenesis in rodents. In this study, the formation and persistence of benzo[a]pyrene (B[a]P)-derived DNA adducts in vivo was determined in the abdominal mammary organs of adult nulliparous and parous BALB/c mice treated orally with the carcinogen. Mammary DNA isolated from animals in both groups revealed only one major adduct on TLC maps by P1-nuclease 32P-postlabeling analysis. The major adduct co-migrated with the (+)-enantiomer of anti-BPDE-dGp. Much lower levels of the (-)-enantiomer were detected. Most of the adduct quantitated was probably contributed by cells of the stromal compartment, since the gland-free organ (cleared fat pad) generated essentially equivalent profiles and level of adduct by 32P-postlabeling. Comparable levels of the B[a]P-derived adduct were observed in the intact mammary organ of both nulliparous and parous mice during a time course from 1 to 28 days after treatment. In both cases, adduct removal occurred exponentially with a half-life of approximately 16 days. The capacity for de novo formation of reactive metabolites by the mammary organ was demonstrated in vitro: digests of DNA from mammary mince exposed to B[a]P generated an adduct on TLC maps that also co-migrated with the (+)-anti-BPDE-dGp standard. Thus, our cumulative findings confirm the capacity of mammary cells to form potentially carcinogenic DNA adducts; however, the functional changes that occur in the mouse mammary gland as a result of parity did not influence the profile, level or persistence of adduct following exposure to a known carcinogen. Other factors, such as changes in mammary cell cycle kinetics or responsiveness to promotional stimuli may be more causally related to reduction in incidence of neoplasia observed in parous animals.

Animals↗

Reactivation of coccidioidomycosis in pregnancy.

A woman presented in the third trimester with a recurrence of coccidioidomycosis. She had been treated 5 years earlier for coccidioidal meningitis. We induced delivery, and both mother and infant had favorable outcomes. We believe that this case represents a reactivation of the previously treated disease.

Adult↗

Epidural anesthesia, episiotomy, and obstetric laceration.

The relationships among epidural anesthesia, forceps use, parity, episiotomy, and laceration were studied in 9493 uncomplicated vertex deliveries of spontaneous onset and normal course. The use of epidural anesthesia was not associated with an increased incidence or severity of birth-canal trauma. Episiotomy was associated with a decreased rate of perineal laceration, but an overall increase in the rate of perineal trauma. The trauma that did occur with episiotomies was four times more likely to be major than that when no episiotomy was performed.

Anesthesia, Epidural↗

Neutral and acidic human tracheobronchial mucin. Isolation and characterization of core protein.

Human bronchial mucin from a patient suffering from chronic bronchitis was solubilized in aqueous solution containing sodium azide and protease inhibitors and purified by Sepharose 4B and 2B column chromatography. The mucin was further purified by cesium bromide density gradient centrifugation. Sodium dodecyl sulfate-polyacrylamide gel (7.5%) electrophoresis of this material showed high-molecular-weight mucin component(s) at the top of the gel. Chemical analysis of this preparation indicated a typical mucin profile of amino acids and carbohydrates. Ion-exchange chromatography resulted in resolution of the purified mucin into neutral and acidic fractions. Comparison of the chemical composition of these two fractions showed higher mole percentage of threonine, serine, sialic acid, and sulfate in the acidic fraction. Chemical deglycosylation of the purified mucin preparation with trifluoromethane sulfonic acid was carried out at 20 degrees C for 3 1/2 h. Sialic acid, fucose, galactose, and N-acetylglucosamine were completely removed, whereas traces of N-acetylgalactosamine were still detected. High-pressure liquid chromatography of the deglycosylated products from native, neutral, and acidic mucin preparations resulted in a principal peptide, P1, with identical amino acid composition. Cyanogen bromide (CNBr) treatment of the peptide P1 from neutral and acidic mucins and subsequent fractionation of the fragments by high-pressure liquid chromatography resulted in similar peptide profiles. The P1 peptide fraction was further subjected to high-pressure liquid chromatography in a second solvent system, which resulted in two peaks, P1a and P1b. Gel filtration of both peptides in 6 M guanidine hydrochloride indicated a single peak with molecular weight of approximately 97 kDa. The amino acid profile of the two peptides was dominated by high levels of threonine, serine, and proline, which combined accounted for nearly 39% of the total residues, and in most respects, the profile resembled that of native mucin. End-group analysis of the peptide P1a indicated a blocked N-terminus, whereas serine was found to be the N-terminal amino acid in the peptide P1b. Rabbit antibodies prepared against the peptide P1 from native tracheal mucin reacted strongly with neutral and acidic mucin as well as the mucin from human colon. Both neutral and acidic human tracheal mucins were immunologically reactive with mouse monoclonal antibody HMPFG-2, which was prepared against human mammary mucin. However, the response of this antibody to human colonic mucin was rather weak.

Amino Acids↗

Multiple DNA adducts in lymphocytes of smokers and nonsmokers determined by 32P-postlabeling analysis.

Identification of DNA adducts in peripheral lymphocytes could serve as a means of monitoring human exposure to potential genotoxic agents. In this study, DNA from peripheral lymphocytes of smokers and nonsmokers was examined for adducts by the P1 nuclease 32P-postlabeling technique. Thin layer chromatography (TLC) maps from both groups revealed multiple DNA adducts which ranged from no adducts for one individual to six adducts for a different individual. The total DNA adduct concentrations were approximately one adduct in 10(8)-10(10) normal nucleotides. Comparison of the adduct TLC profiles revealed individual variation in both pattern and level of DNA adducts. The type and amount of adduct was not influenced by smoking history and remained unchanged in four out of six subjects who were resampled after a 1 month interval. The capacity of lymphocytes to form BaP-derived DNA adducts after a 72 h incubation with 10(-6) M [3H]BaP was measured by both high-performance liquid chromatography (HPLC) and 32P-postlabeling analysis. The in vitro adduct values detected by [3H]nucleoside concentrations on HPLC ranged from 1 to 7 fmol adduct per micrograms DNA (3.3-23.3 adducts per 10(7) nucleotides). The [3H]nucleoside values were consistent with values obtained by 32P-postlabeling of the same sample (correlation coefficient of 0.88). No relationship was apparent between the capacity of lymphocytes to form a [3H]BaP-derived adduct in vitro and the concentration of any adduct, or total adducts present in untreated lymphocytes. These results suggest that multiple DNA adducts are present in lymphocytes from nonsmokers as well as smokers, although the profile and extent of these adducts can vary among individuals. The relationship of the lymphocyte DNA adducts detected in this study to human cancer susceptibility remains to be determined.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

Evaluation of murine placental degradation and transfer of [125I]iodo-epidermal growth factor.

Since epidermal growth factor (EGF) has been postulated to play a role in embryonic and fetal growth, a study was undertaken to assess the placental degradation and transfer of maternally administered EGF. Before iodination, mouse EGF was purified to homogeneity by reversed-phase HPLC. Approximately 5 ng [125I]iodo-EGF (approximately 10(6) cpm) were injected iv into day 10, day 13, or day 17 pregnant CD-1 mice; radioactivity in plasma, placentas, and conceptuses was measured up to 2 h after injection. The time course analysis revealed an initial rapid decline in total plasma radioactivity followed by an increase that was maximal by approximately 30 min. Gel filtration (G-15, G-50) chromatography of plasma revealed that by 5 min, radioactivity was associated with free 125I and with material much larger than EGF. No apparent degradation of [125I]iodo-EGF occurred after direct incubation with maternal plasma. Placental radioactivity had an initial phase of decay between 1 and 5 min followed by an increase that became maximal between 30 and 60 min. Extracts of placentas made with 4 M urea in 0.2 M Tris-HCl, pH 8.0, and taken 1-30 min after injection revealed radioactivity coeluting predominantly with [125I]iodo-EGF at 1 min but shifting to mostly free 125I by 30 min. Uptake of radioactivity by conceptuses was not evident until about 15 min, and only free 125I was detected in extracts; the same results were obtained when 5 micrograms unlabeled EGF were injected simultaneously with [125I]iodo-EGF. Incubation of placental mince with [125I]iodo-EGF yielded [125I]MIT as the apparent major radioactive degradation product. Formation of [125I]MIT in vitro was both time- and temperature-dependent. At 37 C, marked formation of [125I]MIT was observed; at 22 C, only a negligible amount was formed after incubation of mince with [125I]iodo-EGF for 60 min. Incubation of [125I]iodo-EGF with kidney mince yielded predominantly free 125I. When tissues were incubated directly with [125I]MIT, kidney tissue deiodinated the [125I]MIT, but placental tissue did not. When [125I]iodo-EGF was incubated for up to 2 h with kidney tissue in the presence of excess MIT (unlabeled), the major degradation product eluted as [125I]MIT, instead of free 125I. These findings suggest that the mouse placenta can readily bind and then degrade [125I]iodo-EGF to constituent amino acids.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Purification and properties of an oestrogen-stimulated mouse uterine glycoprotein (approx. 70 kDa).

An oestrogen-induced secretory protein from mouse uterine luminal fluid was purified by CM-Affi-Gel Blue chromatography and reverse-phase h.p.l.c. This protein has an apparent molecular mass of approx. 70 kDa both by SDS/polyacrylamide-gel electrophoresis (with or without 2-mercaptoethanol) and by gel-filtration column chromatography, indicating that it exists as a single-chain polypeptide. Further analysis of the protein revealed that it is highly basic (pI greater than or equal to 10) and is a glycoprotein. The N-terminus appears to be blocked to Edman degradation. The partial amino acid sequence of a fragment was obtained by cleavage with CNBr; no sequence homology was apparent between the analysed fragment and other known sequences. The incorporation of [35S]methionine into uterine proteins in vitro revealed that oestrogen treatment of immature mice stimulates both synthesis and secretion of the 70 kDa protein. An enzyme-linked immunosorbent assay with polyclonal antibody was used to determine the tissue distribution of the protein. Tissues such as lung, brain, spleen, muscle, intestine, liver, kidney and ovary of oestrogen-treated mice did not have detectable amounts of the 70 kDa protein. Immunoreactivity was present in uterine and vaginal tissues from oestrogen-treated animals. The 70 kDa protein was not induced by testosterone or progesterone. Although the function of this protein is unknown, it is useful as a marker for the study of oestrogen action in the mammalian uterus as well as regulation of gene expression at the molecular level.

Amino Acid Sequence↗

Beta-epidermal growth factor is the des-asparaginyl form of the polypeptide.

Reversed-phase high performance liquid chromatography of mouse epidermal growth factor (EGF) yielded two major forms, alpha- and beta-EGF, and a minor component, gamma-EGF. All three forms exhibited receptor-binding activity. Analysis of native alpha- and beta-EGF by mass spectrometry and partial Edman degradation led us to propose that alpha-EGF has a primary structure equivalent to that originally reported for EGF and that beta-EGF is the des-asparaginyl form of the polypeptide. When the purified alpha- and beta-polypeptides were cultured with human embryonic palatal mesenchymal cells stimulation of cell proliferation was observed at concentrations as low as 0.01 ng/ml with maximal stimulation occurring at about 1 ng/ml. Essentially no difference was noted in the mitogenic potency of the two forms. This suggests that the NH2-terminal region of EGF is not critical for mitogenic activity.

Amino Acid Sequence↗

Active immunization of prepubertal bulls against testosterone: Seminal and testicular characteristics after puberty.

Twenty-four Holstein bull calves were immunized at 1.0 month of age against either testosterone-17-hemisuccinate-human serum albumin (treated bulls) or against human serum albumin alone (control bulls). Booster injections were given monthly through five months of age. Bulls were reimmunized at six months of age with testosterone-17-hemisuccinate-equine serum albumin (treated bulls) or equine serum albumin alone (control bulls). At 12 months of age, eight treated and eight control bulls were electroejaculated twice daily for two days and then castrated. The remaining four bulls in each group were electroejaculated and castrated at 18 months of age. Active immunization against testosterone significantly elevated the binding of (3)H-testosterone in plasma within four weeks. Body weights of bulls were not affected by treatment. Concentrations of luteinizing hormone (LH) and follicle stimulating hormone (FSH) in plasma were generally not altered by treatment. At castration at 12 months of age, testosterone-immunized bulls tended to have greater (P < 0.15) parenchymal weights and had 30% greater (P < 0.07) daily sperm production (DSP) rates than control bulls; seminal characteristics (motility and intact acrosomes) were not affected. At 18 months of age, testosterone-immunized bulls had 21% greater (P < 0.07) parenchymal weights and 35% greater (P < 0.04) DSP rates than control bulls; again, seminal characteristics were not affected. It appears that prepubertal active immunization against testosterone is a potential means of increasing testicular size and sperm production rates in postpubertal bulls.

Journal Article↗

Effects of placement of intravaginal sponges on LH, FSH, estrus and ovarian activity in mares during the nonbreeding season.

Eight seasonally anestrous mares were administered intravaginal polyurethane sponges on December 15 and then weekly thereafter until February 1. Control mares received no sponges or genital contact. Sponge insertion caused an immediate surge in follicle-stimulating hormone (FSH) concentrations in jugular plasma in 50% of treated mares whereas no control mares had surges in FSH (P less than .05). The effect of treatment on luteinizing hormone (LH) concentrations was much less dramatic and only three treated mares appeared to have positive responses. Sponge-treated mares exhibited positive responses in FSH concentrations 11 times out of 32 mare-days and control mares zero out of 28 (P less than .05). The magnitude of the FSH response decreased rapidly with successive responses. Sponge insertion induced estrus in four of eight treated mares; no control mares exhibited estrus (P less than .05). Sponge insertion also increased ovarian size and the incidence of large follicles. When all mares were fed altrenogest for 14 d beginning February 1, there was no beneficial effect of sponge treatment on number of mares exhibiting estrus or on pregnancy rate. These data confirm earlier speculations that sponge treatment causes surges in gonadotropins and increased ovarian size in approximately 50% of anestrous mares. However, sponge treatment does not appear to provide a practical means of preparing mares for progestogen synchronization during the nonbreeding season.

Animals↗

Effects of testosterone, dihydrotestosterone and estradiol on gonadotropin release after gonadotropin releasing hormone administration in cyclic mares.

Sixteen intact cyclic mares were treated on the fourth day of estrus and then every other day for a total of six injections with 1) testosterone propionate, 2) dihydrotestosterone (DHT) benzoate, 3) estradiol (E2) benzoate or 4) safflower oil. Mares were given gonadotropin releasing hormone (GnRH) on Day 3 of estrus (pretreatment) and again 24 h after the last steroid or oil injection. Treatment with testosterone propionate resulted in a greater (P less than 0.05) follicle-stimulating hormone (FSH) response to the second injection of GnRH compared with all other treatments. Treatment with DHT benzoate also resulted in greater (P less than 0.05) FSH response to GnRH compared with control and E2 benzoate-treated mares. Testosterone propionate and E2 benzoate administration suppressed (P less than 0.05) the normal diestrous rise in FSH concentrations exhibited by the control and DHT benzoate-treated mares. Steroid treatment did not affect the luteinizing hormone (LH) response to GnRH, although testosterone propionate treatment did suppress concentrations of LH in daily blood samples during Days 3 to 6 of treatment. It is concluded that testosterone's effect on FSH after GnRH treatment observed in this and previous experiments can be attributed to two different properties of the hormone or its metabolites acting simultaneously. That is, testosterone increased the secretion of FSH in response to GnRH as did DHT (an androgenic effect). At the same time, testosterone suppressed FSH concentrations in daily blood samples in a manner identical to that of E2 benzoate (an estrogenic effect).

Animals↗

Testosterone administration to mares during estrus: duration of estrus and diestrus and concentrations of LH and FSH in plasma.

To study the possible role of ovarian androgens in regulation of follicle stimulating hormone (FSH) secretion in the cycling mare, five mature, intact mares were treated with testosterone (20 micrograms/kg of body weight) daily during estrus; five control mares received safflower oil on the same schedule. Mares were teased for estrus and samples of jugular blood were drawn daily through one full estrous cycle. Concentrations of FSH in plasma were measured by a newly developed radioimmunoassay based on anti-ovine FSH serum and radioiodinated equine FSH. Testosterone treatment during estrus had no effect on duration of estrus, diestrus or the total cycle. Concentrations of FSH in plasma during estrus were unaffected by testosterone treatment. However, FSH concentrations in testosterone-treated mares were elevated (P less than .05) compared with controls during mid-diestrus (d 6 through 11). The magnitude and timing of the LH peaks were unaffected by treatment, as was the day on which the first elevated progesterone concentration occurred. These data are consistent with a model of FSH secretion in which ovarian androgens cause an accumulation of FSH in the pituitary during estrus in preparation for the surges that occur in FSH secretion during diestrus.

Animals↗

Umbilical-cord plasma progesterone in term infants delivered by caesarean section.

Plasma progesterone concentration was measured by radioimmunoassay in blood samples taken from 67 patients delivered by lower-segment caesarean section (LSCS). Blood samples were taken from umbilical-cord artery and vein and from a peripheral maternal vein. Cord venous progesterone levels were higher (c400 ng/ml) in those patients where the fetus was clinically in jeopardy and this was the principal indication for section. Patients in whom the fetus was not in jeopardy had lower cord venous progesterone concentrations (c300 ng/ml) regardless of whether or not they were in labour. Maternal levels of progesterone were similar in all patients. The advantage to the fetus of these varying progesterone concentrations is not clear, but the evidence lends support to the hypothesis that the fetus exercises control over placental progesterone production during parturition.

Cesarean Section↗