L-Cysteine and Sodium Hydrosulphide Inhibit Spontaneous Contractility in Isolated Pregnant Rat Uterine Strips in vitro

Mechanisms involving the timing of normal parturition are not well understood in most animal species. To gain a greater understanding of the mechanisms, we employed hypoxia to perturb the normal system of parturition. The present study was designed to investigate the effects of chronic hypoxia on myometrial contractility in the near-term pregnant rat. Rats were exposed to room air (control) or to continuous hypoxia (10.5% O2) either from experimental days 19 through 21 (2-day exposure) or from experimental days 15 through 21 (6-day exposure). On day 21, blood was collected for hormone assays, and the uterine horns were collected from each dam. One horn was snap-frozen in liquid nitrogen for oxytocin (OT) receptor analysis, and the other was used for in vitro assessment of myometrial contractile responses to cumulative doses of OT or arginine vasopressin (AVP). Hypoxic exposure resulted in approximately 60% reduction of the maximal myometrial contractile response to OT and a significant reduction in OT binding sites from 256.9 +/- 34.9 to 84.9 +/- 21.3 fmol/mg protein (P<0.01). In contrast, the contractile response to AVP was unaffected after exposure to chronic hypoxia (P> 0.05). Additionally, we observed no difference in the plasma concentrations of estrogen, progesterone, and corticosterone. We conclude that chronic hypoxia decreased the effectiveness of OT-specific contractile mechanisms, at least partially through a decrease in OT binding sites.

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Contrasting effects of DETA/NO, a spontaneously releasing nitric oxide donor, on pregnant rat uterine contractility in vitro and in vivo.

Journal of the Society for Gynecologic Investigation ◽

10.1016/1071-5576(96)82522-6 ◽

1996 ◽

Vol 3 (2) ◽

pp. 96A

Author(s):

C BUHIMSCHI

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Donor ◽

Uterine Contractility ◽

Pregnant Rat

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In vitro myometrial response to aluminum fluoride in the pregnant rat following chronic hypoxia.

Journal of the Society for Gynecologic Investigation ◽

10.1016/1071-5576(96)83016-4 ◽

1996 ◽

Vol 3 (2) ◽

pp. 343A

Author(s):

J RHEE

Keyword(s):

Chronic Hypoxia ◽

Aluminum Fluoride ◽

Pregnant Rat

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Stimulation of contraction of pregnant rat uterus in vitro by non-dechlorinated and microbially dechlorinated mixtures of polychlorinated biphenyls.

Environmental Health Perspectives ◽

10.1289/ehp.01109275 ◽

2001 ◽

Vol 109 (3) ◽

pp. 275-282 ◽

Cited By ~ 15

Author(s):

J Bae ◽

M A Mousa ◽

J F Quensen ◽

S A Boyd ◽

R Loch-Caruso

Keyword(s):

Polychlorinated Biphenyls ◽

Rat Uterus ◽

Pregnant Rat ◽

Stimulation Of

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In vivo and in vitro Ovarian Steroidogenesis in the Pregnant Rat

Biology of Reproduction ◽

10.1095/biolreprod25.4.683 ◽

1981 ◽

Vol 25 (4) ◽

pp. 683-691 ◽

Cited By ~ 61

Author(s):

Kazuyoshi Taya ◽

Gilbert S. Greenwald

Keyword(s):

Pregnant Rat ◽

Ovarian Steroidogenesis

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Urinary excretion of prostacyclin in a rat model of uteroplacental vasculature occlusion: implications for fetal growth retardation

Reproduction Fertility and Development ◽

10.1071/rd9960895 ◽

1996 ◽

Vol 8 (5) ◽

pp. 895 ◽

Cited By ~ 1

Author(s):

M Hophy ◽

S Harel ◽

E Yavin

Keyword(s):

Blood Flow ◽

Urinary Concentration ◽

Fetal Blood ◽

Experimental Conditions ◽

Pregnant Rat ◽

Flow Interruption ◽

Lower Ability ◽

Wet Weight ◽

High Concentrations

An experimental model was devised in the pregnant rat to study by a combined high pressure liquid chromatography and radioimmunoassay technique the accumulation of prostanoids (PNs) in the urine after transient-complete or permanent-partial interruption of the maternal-fetal blood flow. After 8 min of complete restriction of the blood flow in the pregnant rat at 18 days of gestation, the urinary concentration of 6-keto-prostaglandin F1 alpha (6k-PGF1 alpha, the stable prostacyclin metabolite) increased from 4.97 +/- 1.27 ng mg-1 creatinine to 8.09 +/- 2.47 ng mg-1 creatinine and 13.02 +/- 4.5 ng mg-1 creatinine after the second and third post-operative day respectively. The urinary concentration of the 2,3-dinor derivative of prostacyclin reached 12.35 +/- 5.44 ng mg-1 creatinine after the second post-operative day and was reduced to 4.71 +/- 1.94 ng mg-1 creatinine after the third post-operative day. The concentration of thromboxane B2 (TxB2, the stable thromboxane A2 metabolite) increased approximately 7-fold and 13-fold over that of the control after the second and third post-operative day respectively. The urinary concentration of the 2,3-dinor derivative of TxB2 (d-TxB2) increased from about 1.42 +/- 0.3 ng mg-1 creatinine to 4.49 +/- 0.9 ng mg-1 creatinine and 7.76 +/- 2.63 ng mg-1 creatinine under the same experimental conditions. Increases in the urinary concentrations of 6k-PGF1 alpha and d-TxB2 to 94 +/- 27.76 ng mg-1 creatinine and 12.05 +/- 2.26 ng mg-1 creatinine, respectively, were observed on the second post-operative day, after the restriction time was increased to 30 min. Permanent-partial occlusion of the maternal fetal circulation resulted in excretion of PNs in the urine to similar levels produced after transient-complete restriction. High concentrations of prostacyclin (range, 0.8 ng min-1 mg-1 wet weight) were produced in vitro by uterine preparations from restricted animals after the second post-operative day. Placenta preparations from restricted animals generally exhibited a lower ability to synthesize PNS (up to 0.006 ng min-1 mg-1 wet weight) compared with uterine tissue but produced more thromboxane than their sham counterparts. The data suggest that the uterus constitutes the main source for urinary PN excretion following short episodes of maternal-fetal blood flow interruption.

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Poorly controlled diabetes mellitus alters placental structure, efficiency, and plasticity

BMJ Open Diabetes Research & Care ◽

10.1136/bmjdrc-2020-001243 ◽

2020 ◽

Vol 8 (1) ◽

pp. e001243

Author(s):

Jackson Nteeba ◽

Kaela M Varberg ◽

Regan L Scott ◽

Mikaela E Simon ◽

Khursheed Iqbal ◽

...

Keyword(s):

Diabetes Mellitus ◽

Fetal Development ◽

Trophoblast Invasion ◽

Ambient Conditions ◽

Placental Development ◽

Junctional Zone ◽

Pregnant Rat ◽

Elevated Glucose ◽

The Impact

IntroductionThe hemochorial placenta provides a critical barrier at the maternal–fetal interface to modulate maternal immune tolerance and enable gas and nutrient exchange between mother and conceptus. Pregnancy outcomes are adversely affected by diabetes mellitus; however, the effects of poorly controlled diabetes on placental formation, and subsequently fetal development, are not fully understood.Research design and methodsStreptozotocin was used to induce hyperglycemia in pregnant rats for the purpose of investigating the impact of poorly controlled diabetes on placental formation and fetal development. The experimental paradigm of hypoxia exposure in the pregnant rat was also used to assess properties of placental plasticity. Euglycemic and hyperglycemic rats were exposed to ambient conditions (~21% oxygen) or hypoxia (10.5% oxygen) beginning on gestation day (gd) 6.5 and sacrificed on gd 13.5. To determine whether the interaction of hyperglycemia and hypoxia was directly altering trophoblast lineage development, rat trophoblast stem (TS) cells were cultured in high glucose (25 mM) and/or exposed to low oxygen (0.5% to 1.5%).ResultsDiabetes caused placentomegaly and placental malformation, decreasing placental efficiency and fetal size. Elevated glucose disrupted rat TS cell differentiation in vitro. Evidence of altered trophoblast differentiation was also observed in vivo, as hyperglycemia affected the junctional zone transcriptome and interfered with intrauterine trophoblast invasion and uterine spiral artery remodeling. When exposed to hypoxia, hyperglycemic rats showed decreased proliferation and ectoplacental cone development on gd 9.5 and complete pregnancy loss by gd 13.5. Furthermore, elevated glucose concentrations inhibited TS cell responses to hypoxia in vitro.ConclusionsOverall, these results indicate that alterations in placental development, efficiency, and plasticity could contribute to the suboptimal fetal outcomes in offspring from pregnancies complicated by poorly controlled diabetes.

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Hormonal control of Luteal 20α-Hydroxy steroid dehydrogenase and Δ5-3β-hydroxy steroid dehydrogenase during luteolysis in the pregnant rat

Biochemical Journal ◽

10.1042/bj1520433a ◽

1975 ◽

Vol 152 (3) ◽

pp. 433-443 ◽

Cited By ~ 8

Author(s):

R G Rodway ◽

N J Kuhn

Keyword(s):

Prostaglandin F2α ◽

Late Pregnancy ◽

Normal Pregnancy ◽

Hormonal Control ◽

Placental Lactogen ◽

Pregnant Rats ◽

Pregnant Rat ◽

Hydroxy Steroid ◽

Steroid Dehydrogenase

Treatment of pregnant rats with human chorionic gonadotrophin, luteotrophin (luteinizing hormone), luteotrophin-releasing hormone, prostaglandin F2α, aminoglutethimide, or by foetoplacental removal or hysterectomy achieved a common multiple-response pattern, namely increased activity of luteal 20α-hydroxy steroid dehydrogenase with decreased activity of delta5-3β-hydroxy steriod dehydrogenase and release of delta4-3-oxo steroids in vitro. 2. Similar effects of foetoplacental removal are noted in pregnant mice. 3. Gonadotrophin induced lower activities of 20α-hydroxy steroid dehydrogenase, except at the very end of pregnancy, and partly inhibited the induction caused by foetoplacental removal. 4. The results suggest that existence of a placental factor that restrains these changes until the end of normal pregnancy, which is produced in amounts proportional to the number of placentae and is conveyed to the ovary via the blood. 5. This factor was not replaced by prolactin. 6. It is argued that neither placental lactogen nor pituitary luteotrophin participate in the induction of 20α-hydroxy steroid dehydrogenase at late pregnancy in the rat. 7. Aminoglutethimide induced 20α-hydroxy steroid dehydrogenase only in late pregnancy. This was partly reversed by progesterone, wholly reversed by progesterone plus oestrogen, and did not involve the pituitary.

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