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At least 73 records · Page 4Linked to original sources
PubMed2001

[Reproductive and developmental toxicity studies of S-1090, cefmatilen hydrochloride hydrate (1)--A study on oral administration prior to and in the early stages of pregnancy in rats].

Cefmatilen hydrochloride hydrate (S-1090) was administered daily by gavage to rats at doses of 100, 300 or 1000 mg potency/kg/day prior to and in the early stage of pregnancy to assess its adverse effects on parental reproductive ability and embryo-fetal development. Loose and/or reddish brown feces were observed in both males and females of all the S-1090 dosing groups, and abdominal distention was also observed in males throughout the dosing period. No drug-related deaths occurred in either males or females. In males, body weight and food consumption were increased at a dose of 1000 mg potency/kg/day throughout the dosing period. In females, body weight gain was restrained during late pregnancy, and food consumption was decreased transiently following the initiation of dosing, and then remained high on the day before parturition in all the S-1090 dosing groups. Necropsy of male and female rats revealed an increase in the cecum weight. The reproductive ability of males and females was normal in all the S-1090 dosing groups. No effects of S-1090 were observed in the implantation ratio, embryo-fetal viability, fetal body weight, and incidence of external, skeletal and visceral anomalies. Based on these results, the no observed adverse effect levels of S-1090 are estimated to be less than 100 mg potency/kg/day for parental general toxicity, 1000 mg potency/kg/day for reproductive toxicity, and 1000 mg potency/kg/day for developmental toxicity in embryo-fetuses under the conditions of the present study.

Administration, Oral↗
PubMed2005

Understanding cellular disruptions during early embryo development that perturb viability and fetal development.

An inability to regulate ionic and metabolic homeostasis is related to a reduction in the developmental capacity of the embryo. The early embryo soon after fertilisation and up until compaction appears to have a reduced capacity to regulate its homeostasis. The reduced ability to regulate homeostasis, such as intracellular pH and calcium levels, by the precompaction-stage embryo appears to impact on the ability to regulate mitochondrial function and maintain adequate levels of energy production. This reduction in ATP production causes a cascade of events leading to disrupted cellular function and, perhaps ultimately, disrupted epigenetic regulation and aberrant placental and fetal development. In contrast, after compaction the embryo takes on a more somatic cell-like physiology and is better able to regulate its physiology and therefore appears less vulnerable to stress. Therefore, for human IVF it would seem important for the establishment of healthy pregnancies that the embryos are maintained in systems that are designed to minimise homeostatic stress, particularly for the cleavage-stage embryos, as exposure to stress is likely to culminate in impaired embryo function.

Adenosine Triphosphate↗
PubMed1978

Real-time sonography in obstetrics.

Three hundred fifty real-time scans were performed on pregnant women for various indications. Placental localization was satisfactorily obtained in 173 of 174 studies. Estimates of fetal gestation from directly measured biparietal diameter were +/-2 weeks of actual gestation in 153 of 172 (88.9%) measurements. The presence or absence of fetal motion and cardiac activity established a diagnosis of fetal viability or fetal death in 32 patients after the first trimester. Accurate diagnosis was made in 52 of 57 patients with threatened abortions, and two of these errors occurred in scans performed before completion of the eighth postmenstrual week. Because of the ability to demonstrate fetal motion, real-time sonography should have many applications in obstetrics.

Abortion, Threatened↗
PubMed1986

Sarcoma complicating pregnancy.

An unusual case of pregnancy complicated by intraabdominal sarcoma is presented; tumor reductive surgery was required late in the second trimester so that a gestational age of fetal viability could be reached. Fetal outcome was successful. The mother died shortly after delivery. Management of widespread intraabdominal cancer complicating the latter half of pregnancy should aim toward obtaining fetal viability.

Abdominal Neoplasms↗
PubMed2006

Endothelin and platelet-activating factor: significance in the pathophysiology of ischemia/reperfusion-induced fetal growth restriction in the rat.

OBJECTIVE: The objective of the study was to evaluate the role of endothelin-1 and platelet-activating factor in ischemia/reperfusion-induced fetal growth restriction in the rat. STUDY DESIGN: On day 17 of gestation, the right uterine and ovarian arteries were occluded for 30 minutes in experimental but not sham-operated rats. All rats received endothelin receptor A antagonist, A-127722 (10 mg/kg per day), platelet-activating factor antagonist, WEB-2086 (1 mg/kg), or vehicle. On gestational day 21, litter size, fetal viability, and fetal and placental weights were recorded. Reverse transcription-polymerase chain reaction for phospholipase A2-IIA and preproendothelin-1 messenger ribonucleic acid was performed on uterus and placentas from each uterine horn. Groups were compared statistically by analysis of variance. RESULTS: Ischemia/reperfusion reduced fetal weights, in both the ischemic horn and the nonischemic horn (P < .001). Antagonism of either endothelin receptor A or platelet-activating factor normalized fetal growth in both horns. Neither placental weight nor the incidence of fetal demise was affected by ischemia/reperfusion. Phospholipase A2-IIA and preproendothelin-1 messenger ribonucleic acid expression did not differ between right and left uterine horns in any group. Uterine and placental tissues in the ischemia/reperfusion group exhibited increased phospholipase A2-IIA (P < .01) but not preproendothelin-1. CONCLUSION: Endothelin-1 and platelet-activating factor are both important mediators in the pathophysiology of ischemia/reperfusion-induced fetal growth restriction in the rat, contributing to the fetal growth restriction observed in both the ischemic and nonischemic horns. Antagonism of either mediator produces normal fetal growth in this model of fetal growth restriction.

Animals↗
PubMedDate not supplied

Teratogenic potential of FD&C Red No. 3 when given by gavage.

FD&C Red No. 3 (erythrosine) is a commonly used food additive. As part of a series of studies on the potential fetal developmental effects of food colors, FD&C Red No. 3 was administered by gavage to pregnant Osborne-Mendel rats at daily dose levels of 15, 30, 100, 200, 400, or 800 mg/kg on days 0-19 of gestation. Control animals were given distilled water by gavage. On gestation day 20, the animals were euthanized and cesarean sections were performed. During the entire treatment period, feed consumption by the animals given 400 mg/kg doses was increased significantly; the increases in the animals given 30 or 800 mg/kg were of borderline significance. The only significant increase in maternal weight gain, on days 0-7 in the animals given 30 mg/kg, was considered a random occurrence. No dose-related changes were seen in maternal clinical findings, implantations, fetal viability, or fetal size (weight and length). No fetal terata were seen, and neither skeletal nor visceral development was affected. FD&C Red No. 3 was neither fetotoxic nor teratogenic at 800 mg/kg when given by gavage.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Developmental toxicity of Orange B given to rats in drinking water.

Orange B, a pyrazolone dye used to color frankfurter and sausage casings, was given in distilled drinking water to pregnant Osborne-Mendel rats throughout gestation. Assessed on the basis of fluid consumption, the dose levels of 0, 0.05, 0.1, 0.2, and 0.4% corresponded to daily Orange B consumption of 0, 67.5, 129.6, 266.6, and 532.3 mg/kg body weight, respectively. On gestation day 20, the females were euthanized and cesarean sections were performed. Throughout gestation, the treated animals consumed less fluid than did the controls, but the decreases were not dose-related. Feed consumption and maternal weight gain were not affected. No dose-related changes were seen in maternal clinical findings, implantations, fetal viability, or fetal size (weight and length). No compound-related effects were seen in sternebral development. Ossification of the interparietal bones was reduced at some dose levels, but the decreases were considered random because of absence of dose response. No dose-related effect was seen in the incidence of skeletal variations in fetuses or in the number of litters containing fetuses with skeletal variations. Skeletal development, as measured by the average number of ossified vertebrae, was similar in all groups. Soft-tissue development was not affected by dose levels of 0.05 to 0.2%. In animals treated with 0.4% Orange B, significant increases were seen in the incidence of hydroureters (severe and moderate), in the average numbers of fetuses with at least one and at least two soft-tissue variations per litter, and in the percentage of litters containing fetuses with at least two soft-tissue variations.

Administration, Oral↗
PubMedDate not supplied

Developmental toxicity of orange B when given to rats by gavage.

The pyrazolone dye Orange B was given by gavage to pregnant Osborne-Mendel rats throughout gestation. Dose levels of 0, 15, 30, 100, 200, 400, or 700 mg/kg body weight were given daily. On gestation day 20, the females were killed and cesarean sections were performed. Feed consumption and maternal weight gain were not affected. No dose-related changes were seen in maternal clinical findings, implantations, fetal viability, or fetal size (weight and length). No compound-related effects were seen in sternebral development. No dose-related effect was seen in the incidence of skeletal variations in fetuses or in the number of litters containing fetuses with skeletal variations. Skeletal development, as measured by the average number of ossified vertebrae, was similar in all groups. No compound-related effects were seen in soft-tissue development.

Administration, Oral↗
PubMed1976

Ultrasonic diagnosis of intrauterine fetal death.

When there is doubt concerning fetal viability, the confirmation or exclusion of fetal death assumes major importance in the management of pregnancy. Frequently the clinical diagnosis is uncertain and recourse must be had to ancillary investigation. Radiologic methods may confirm the clinical suspicion of intrauterine fetal death in many cases, but these are accompanied by the hazard of irradiation. Ultrasound can provide valuable information regarding fetal viability. Ultrasonic signs of fetal death are discussed in the light of the literature and our own experience, with emphasis on the value of the M-mode in detecting fetal heart pulsations.

Female↗
PubMed2005

Maternal brain death and somatic support.

Brain death is a concept used in situations in which life-support equipment obscures the conventional cardiopulmonary criteria of death, and it is legally recognized in most countries worldwide. Brain death during pregnancy is an occasional and tragic occurrence. The mother and fetus are two distinct organisms, and the death of the mother mandates consideration of the well-being of the fetus. Where maternal brain death occurs after the onset of fetal viability, the benefits of prolonging the pregnancy to allow further fetal maturation must be weighed against the risks of continued time in utero, and preparations must be made to facilitate urgent cesarean section and fetal resuscitation at short notice. Where the fetus is nonviable, one must consider whether continuation of maternal organ supportive measures in an attempt to attain fetal viability is appropriate, or whether it constitutes futile care. Although the gestational age of the fetus is central to resolving this issue, there is no clear upper physiological limit to the prolongation of somatic function after brain death. Furthermore, medical experience regarding prolonged somatic support is limited and can be considered experimental therapy. This article explores these issues by considering the concept of brain death and how it relates to somatic death. The current limits of fetal viability are then discussed. The complex ethical issues and the important variations in the legal context worldwide are considered. Finally, the likelihood of successfully sustaining maternal somatic function for prolonged periods and the medical and obstetric issues that are likely to arise are examined.

Abortion, Therapeutic↗
PubMed1999

Annexin V is critical in the maintenance of murine placental integrity.

OBJECTIVES: Recurrent fetal loss can be a consequence of placental thrombosis, frequently occurring in autoimmune disorders such as antiphospholipid syndrome. A potent anticoagulant, annexin V, is abundant in placental tissues. We investigated the role of annexin V in maintaining fetal viability. STUDY DESIGN: Sites of annexin V activity in placenta were found and neutralized, and the physiologic consequences on fetal development were evaluated. To find extracellular binding sites for annexin V on placental membrane, 2 approaches were taken. An epitope-tagged recombinant annexin V was infused into pregnant BALB/c mice. Endogenous annexin V was evaluated by immunohistochemical techniques. To define a role for annexin V during pregnancy, annexin V was neutralized by tail-vein infusion of affinity-purified anti-annexin V antibodies immediately before mating, 16 hours before the vaginal plugs were observed. Fetal viability, number, and size were evaluated at days 11 or 15 after conception. RESULTS: Endogenous annexin V is enriched along the apical surfaces of trophoblasts. Animals infused with epitope-tagged annexin V had confirmed presence of extracellular binding sites for annexin V exclusively along these surfaces. In mice infused with anti-annexin V antibodies, various degrees of fetal absorption were observed. Thrombosis and necrosis were present in the fetal component of placentas from partially absorbed embryos. Focal necrosis and fibrosis were present in the decidua of placentas from embryos that were significantly smaller than the normal embryos in the same uterus. CONCLUSIONS: Apical surfaces of syncytiotrophoblasts in the placenta possess annexin V binding sites. The binding of annexin V to these coagulation-promoting surfaces is crucial for the maintenance of blood flow through the placenta and consequently for fetal viability. Infusion of anti-annexin V antibodies decreased the availability of annexin V to bind to the trophoblast surfaces and caused placental thrombosis, necrosis, and fetal loss. Our study suggests that anti-annexin V autoantibodies may contribute to recurrent pregnancy failure resulting from placental thrombosis, as found in patients with certain autoimmune diseases.

Abortion, Spontaneous↗
PubMedDate not supplied

The selective estrogen receptor modulator, raloxifene: segment II studies in rats and rabbits.

Raloxifene is a nonsteroidal, selective estrogen receptor modulator developed by Eli Lilly and Company primarily as a therapeutic agent for postmenopausal osteoporosis. Two Segment II studies were conducted that examined maternal reproductive parameters and fetal outcome following gestational exposure to raloxifene. Pregnant CD rats (25/group) and New Zealand white rabbits (20/group) were dosed once daily by oral gavage with 0, 0.1, 1, or 10 mg/kg on Gestation Days (GD) 6 through 17 and 7 through 19, respectively. Maternal body weight and food consumption were monitored throughout pregnancy. Caesarean sections were performed on GD 20 and GD 28 for rats and rabbits, respectively, to evaluate fetal viability, weight, and morphology. In rats, maternal body weight, body weight gain, and food consumption were reduced in all raloxifene treatment groups. Fetal viability was depressed in the 10-mg/kg group and was often associated with signs of hemorrhaging from the vagina. Fetal growth retardation was indicated in the 1- and/or 10-mg/kg groups by increased incidences of fetal runts and the developmental deviations, wavy ribs and kidney cavitation. There was no evidence of treatment-related malformations in rat fetuses. In rabbits, depressions in body weight gain and food consumption occurred in the 10-mg/kg group, and a single abortion occurred in the 1-mg/kg group. Fetal viability and weights were not affected in any of the raloxifene treatment groups. The overall proportions of fetuses with malformations, deviations, or variations were not affected by treatment with raloxifene; however, one fetus each from the 0.1-, 1-, and 10-mg/kg groups had incomplete closure of the interventricular septum. Therefore, maternal and fetal no-effect levels were not obtained in this study of raloxifene.

Administration, Oral↗
PubMed1995

Developmental toxicity of amesergide administered by gavage to CD rats and New Zealand white rabbits.

Amesergide is a selective serotonin 5-HTIC/2 receptor antagonist being developed for the treatment of depression. The potential developmental toxicity of amesergide was evaluated in CD rats and New Zealand white rabbits. Pregnant rats and rabbits were dosed once daily by gavage on Gestation Days 6-17 and 6-18, respectively. Doses for rats were 0, 3, 10, and 30 mg/kg; doses for rabbits and 0, 0.2, 2, and 15 mg/kg. Cesarean sections were performed on rats and rabbits on Gestation Days 20 and 28, respectively. In rats, maternal effects expressed as depression of body weight gain and food consumption were observed at the 30 mg/kg dose level. Fetal viability and morphology were not affected at any dose level. Fetal weight was depressed at the 30 mg/kg dose level. The no-observed-effect level (NOEL) in the rat was 10 mg/kg. In rabbits, maternal effects expressed as a decrease in food consumption occurred at the 2 and 15 mg/kg dose levels; weight gain was depressed at 15 mg/kg. Fetal viability, weight, and morphology were not affected at any dose level. The NOELs for maternal and developmental effects in the rabbit were 0.2 and 15 mg/kg, respectively.

Abnormalities, Drug-Induced↗
PubMed2004

Fetal death: comparative aspects in large domestic animals.

Although the majority of pregnancy failures occur during the embryonic period, reports indicate that approximately 5% of detected pregnancies are lost during the fetal period, underlining the fact that fetal death is a substantial cause of economic loss. However, examination for fetal development or death during pregnancy is not performed routinely in domestic animals, and reference curves for normal fetal growth are, therefore, scarce. In this paper, the numerous possible causes of fetal death are reviewed briefly, with emphasis on the role of placental problems in fetal death and impaired fetal viability. In this respect, the role of placental insufficiency as a cause of pregnancy loss in twin pregnancies in monotocous species is well known, whereas the abnormal placental development leading to retarded fetal growth during pregnancies in recipients of in vitro produced (IVP) or nuclear transfer (NT) embryos has been less extensively documented. Fetal viability or death can be evaluated using hormonal, chemical and ultrasonographic parameters. For example, the viability of the feto-placental unit can be examined by measuring maternal plasma concentrations of oestrone sulphate or the placental proteins, including pregnancy-associated glycoprotein (PAG) and pregnancy-specific protein B-60 (PSPB-60). Low concentrations of any of these three indicate either no pregnancy, or if pregnancy was confirmed earlier, fetal death and abnormally high or low levels can indicate fetal abnormality. Ultrasound can be used to examine the fetal heart rate (FHR), the incidence of fetal movements (FM), the appearance of fetal fluids and the development of the fetus and placenta. However, although abnormal FHRs have been correlated to subsequent fetal death, it is important to remember that there is a large physiological variation in FHR at the end of gestation, due to different behavioural states and differences in FM patterns. Although monitoring fetal viability and death using hormonal and ultrasonographic evaluations is possible during pregnancy in domestic animals, there is considerable physiological variations in the 'normal' values. Therefore, suitable combinations of tests need to be identified and more accurate reference values generated before such approaches can be considered reliable for monitoring the status of individual fetuses.

Animals↗
PubMed1995

Developmental toxicity of dinitroaniline herbicides in rats and rabbits. I. Trifluralin.

The potential developmental toxicity of trifluralin was evaluated in rats and rabbits. Pregnant rats and rabbits were dosed once daily by gavage on Gestation Days 6-15 and 6-18, respectively. Doses for rats were 0, 100, 225, 475, or 1000 mg/kg; doses for rabbits were 0, 100, 225, or 500 mg/kg. Cesarean sections were performed on rats and rabbits on Gestation Days 20 and 28, respectively. In rats, maternal toxicity was indicated in the 475 and 1000 mg/kg treatment groups by depression of body weights and food consumption. Fetal viability and morphology were not adversely affected at any dose level. Developmental toxicity was indicated at the 1000-mg/kg dose level by depression of fetal weight. The NOAEL for maternal toxicity in the rat was 225 mg/kg; the NOAEL for developmental toxicity in the rat was 475 mg/kg. In rabbits, maternal toxicity was indicated at the 225 and 500 mg/kg dose levels by abortions and/or deaths in conjunction with anorexia and cachexia. Developmental toxicity was indicated at the 500 mg/kg dose level by depressed fetal viability and weight. Fetal morphology was not adversely affected at any dose level. The NOAELs for maternal and developmental toxicity in the rabbit were 100 and 225 mg/kg, respectively. Based on these data, trifluralin did not exhibit selective toxicity toward the developing conceptus.

Aniline Compounds↗
PubMed1983

Growth, differentiation, and viability of fetal rat cortical and spinal cord implants into adult rat spinal cord.

Successful transplantation of the fetal brain into adult host brain has been accomplished. These studies explore the growth, differentiation, and viability of E11, E12, and E15 rat fetal cortex and fetal spinal cord implantation into the spinal cord of adult rats (donor and host, Sprague-Dawley). Under deep Chloropent anesthesia, 70 rats had 1-mm cubes of fetal cortex inserted with pressure or by stylus injection subpially between the dorsal horn and dorsal column (left side), or implantation of whole segments of fetal spinal cord. Animals were prepared for light microscopy 14 and 21 days and 1, 2, and 3 months later. Implants by both fetal tissues had a 69% survival rate. The younger the fetal implant the higher the success of the implant (E11 greater than E15). The diameter of fetal spinal cord implants reached the diameter of control postnatal animals after 30 days. The implants not only increased in mass (up to 7-fold in some cases) but differentiated and matured (apolar, unipolar, bipolar, and multipolar) neurons were observed one to three months postimplantation. By 30 days postimplantation, fetal neurons had large, often crenated nuclei, with a large single prominent nucleolus. The most successful implants were the young E11 fetal spinal cord into the adult host spinal cord. These implants represent an initial successful transplantation of fetal spinal cord into adult spinal cord.

Animals↗