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At least 181 records · Page 10Linked to original sources

PubMed1999

Bombesin inhibits apoptosis in developing fetal rat lung.

We have shown recently that apoptosis occurs during fetal and postnatal lung development. Our hypothesis that branching morphogenesis occurs through a delicate balance of cell proliferation and apoptosis predicts that substances that enhance branching of the airways would affect both cell proliferation and apoptosis in the lung. Bombesin-like peptides have a mitogenic effect on bronchial epithelium and fibroblasts, and bombesin has been shown to enhance branching morphogenesis in fetal lung. We used organ cultures of 16-day gestation fetal rat lung to study the effects of bombesin on apoptosis. Cultures were incubated in serumless medium alone or exposed to 1microM bombesin for 0-48 h. Levels of apoptosis were quantified using the TUNEL assay and expressed as percentage of apoptotic cells in paraffin sections of explants. Bombesin significantly inhibited apoptosis in fetal lung mesenchyme 48 h in culture by more than 50% (p < 0.05). The effects of bombesin on apoptosis were prevented completely if explants were exposed to the specific bombesin receptor antagonist, [D-Phe12]bombesin. To examine if the absence of serum in the media could have accounted for some of these effects, explants were cultured for 48 h in serumless medium, medium containing 10% fetal bovine serum, serumless medium with 1 microM bombesin, or medium containing both 10% fetal bovine serum and 1 microM bombesin. The addition of fetal bovine serum to the media reduced apoptosis significantly. The effect of fetal bovine serum on apoptosis was additive with bombesin. We conclude that bombesin inhibits apoptosis in developing fetal rat lung mesenchyme through its interaction with the bombesin receptor.

Animals↗

PubMed1985

[Rat aldolase isozyme gene: structure and expression in the liver during both fetal development and chemical carcinogenesis].

Changes in the gene expression of aldolase A and B isozymes in rat liver during both fetal development and chemical carcinogenesis were analyzed using cDNA probes. The structure of the rat aldolase B gene was also determined, and was discussed in relation to its expression.

Animals↗

PubMed2001

Fetal aortic blood flow assessment from the relationship between fetal aortic diameter pulse and flow velocity waveforms during fetal development.

BACKGROUND: Blood flow is calculated from mean velocity across the vessel and its cross-sectional area and is related to the fetal growth. AIM: To investigate the relationship between diameter pulse waveform (DPW) and flow velocity waveform (FVW) in the fetal descending aorta during fetal development. STUDY DESIGN: Doppler ultrasound and a phase-locked loop echo tracking system were used to measure the FVW and DPW in the fetal descending aorta, respectively. SUBJECTS: We studied 137 normal-growth fetuses (normal group, 20-40 weeks) and 51 fetuses with high umbilical artery pulsatility index (umbilical placental insufficiency, UPI group, 26-40 weeks). OUTCOME MEASURES: We measured the systolic (Sd), diastolic (Dd) diameters, time diameter integral (TDI) and time velocity integral (TVI) and then calculated the TVI x TDI and TVI to TDI ratio. RESULTS: Normal fetal growth was associated with an increase in Sd, Dd, pulse amplitude, TVI, TDI and TVI x TDI. The FVW began to resemble the DPW with decreasing downstream resistance produced by growth of the placenta. The TVI was increased relative to the TDI. The differences in Sd, Dd, TDI and TVI x TDI between the normal and UPI groups were not significant. The TVI was decreased relative to the TDI. There was a decrease in the TVI as a ratio of the TDI. The Dd per unit fetal weight was high in the compromised fetuses. Fetal outcome was examined in relation to the TVI to TDI ratio. Those with a low ratio (below 10th centile) exhibited significantly more adverse indices of fetal outcome. CONCLUSIONS: In fetal compromise there is an increase in diastolic pressure in association with high placental resistance, which causes a major increase in afterload. The efficient circulation associated with fetal growth might be represented by an increase in the ratio of the TVI to the TDI (an index of efficient circulation) when these waveform shapes resemble each other.

Adult↗

PubMed1984

Reproduction and fetal development in rats exposed to nitrous oxide.

The effects of 24 hours of nitrous oxide exposure on reproductive indices and fetal development were examined in Sprague-Dawley rats. Four different experiments employing four concentrations of nitrous oxide--0.75%, 7.5%, 25% and 75%--established that the threshold of toxicity was greater than 25%. At 75% nitrous oxide there was a significant increase in early and late resorptions, and a consistent teratogenic effect (e.g., runts, ocular malformations, limb deformities). Neither the stress of shipping dams while pregnant nor the withholding of food during nitrous oxide exposure resulted in additional adverse effects. Exposure to 25% nitrous oxide was associated with increased deoxyuridine suppression values; however, adverse reproductive effects were not seen at this nitrous oxide concentration. The results of this and other studies which have examined the reproductive and teratogenic effects of nitrous oxide do not contraindicate its use in operating rooms nor, when necessary, as an anesthetic for pregnant surgical patients.

Abnormalities, Drug-Induced↗

PubMed1992

Rat lung polycholorinated biphenyl-binding protein: effect of glucocorticoids on the expression of the Clara cell-specific protein during fetal development.

Certain metabolites of polychlorinated biphenyls (PCBs) are retained in the Clara cells and in the airway lumen of rodent lung due to their interaction with a secretory 13-kDa protein. The expression of this Clara cell-specific, PCB-binding protein (PCB-BP) during the fetal development of the rat lung was studied by means of ligand binding and a monospecific antiserum. The PCB-BP and specific 4,4'-bis([3H]methylsulfony)-2,2',5,5'-tetrachlorobiphenyl binding was first detected on gestational Day 19 and subsequently the levels of PCB-BP and specific ligand binding increased as a function of gestational age. The start site of transcription for the rat PCB-BP gene was determined by primer extension analysis and the information thus obtained was used to develop a quantitative assay for the corresponding mRNA based on solution hybridization and S1 nuclease mapping. The appearance of PCB-BP mRNA during fetal lung development preceded the detection of immunoreactive protein and ligand binding by 1 day. By Day 21, the level of PCB-BP mRNA was 15 ng/100 micrograms total lung RNA which is approximately 30-40% of adult levels. In utero exposure to the synthetic glucocorticoid betamethasone was shown to increase specific 4,4'-bis([3H]methylsulfonyl)2,2',5,5'- tetrachlorobiphenyl binding, PCB-BP protein, and PCB-BP mRNA if administered from gestational Day 18 and onward. By Days 21-22, glucocorticoid treatment resulted in a two- to threefold increase in the levels of specific ligand binding, immunoreactivity, and mRNA, i.e., to approximately adult levels.

Animals↗

PubMed2006

Cell cycle and cell death regulation of neural progenitor cells in the 5-azacytidine (5AzC)-treated developing fetal brain.

In the developing brain, neural progenitor cells are susceptible to many extrinsic stresses, including DNA damage. We treated pregnant rats with 5-azacytidine (5AzC), a DNA demethylating and damaging agent, to investigate the cellular responses of the fetal brain, focusing on the regulation of proliferation and cell death. 5AzC first induced the accumulation of cells in abnormal mitosis, G2-phase accumulation, and then apoptosis of the neural progenitor cells. Most of the apoptotic cells were in G1 phase. Cell cycle transition studies suggested that G2/M progression was blocked, after which the cells moved to G1 phase or underwent apoptosis. p53, a key factor for response to DNA damage, and some of its target genes showed increased expression in Western blot and DNA microarray analyses. In 5AzC-treated fetal brains of p53-deficient mice, apoptosis did not occur, although G2/M accumulation was induced. These results suggest that, in the developing brain, apoptosis is p53-dependent but that another mechanism governs the G2/M checkpoint. The G2/M regulator, Cdc2, was activated by dephosphorylation through G2/M accumulation, suggesting accelerated entry into mitosis leading to accumulation of cells showing abnormal mitosis. Furthermore, some cells may have died due to mitotic catastrophe. Throughout brain development, various cell cycle and cell death regulation mechanisms provide neural progenitor cells with options for defense from DNA damage.

Animals↗

PubMed1996

Expression and distribution of the receptors for coxsackievirus B3 during fetal development of the Balb/c mouse and of their brain cells in culture.

This study was designed mainly to determine the relationships between the expression and distribution of the cellular receptor proteins for coxsackievirus B3 (CVB3) and susceptibility of mouse brain cells during fetal development of Balb/c mice. Immunoblot analysis of fetal extracts demonstrated that the CVB3 receptor proteins were first expressed at day 14 of the fetal stage, and that maximal expression of the cellular receptor occurred at near term or newborn stage. Results also suggested that newborn mouse brain tissue expressed much larger quantities of viral receptor proteins, compared to other tissues. In vitro studies showed that both mouse neurons and astrocytes could be infected by two CVB3 strains, pantropic CVB3 Nancy strain (CVB3N) and myocardiotropic CVB3 Woodruff strain (CVB3W). CVB3N, however, replicated and grew to high titer in primary astrocyte cultures and in primary neuron cultures, whereas, primary astrocyte cultures were relatively resistant to CVB3W. Virus binding assays revealed that CVB3N bound faster and in greater amounts to mouse brain cells than CVBW. These two virus strains, however, were found to share the same receptor specificity by virus competition assays. The number of virus binding sites for CVB3 on newborn mouse brain cells was approximately 1.8 x 10(4) per cell. The data suggested that preferential expression of the cellular receptors on newborn mouse brain cells may be related to their high susceptibilities to CVB3 infection.

Animals↗

PubMed1989

Membrane domains of intestinal epithelial cells: distribution of Na+,K+-ATPase and the membrane skeleton in adult rat intestine during fetal development and after epithelial isolation.

The organization of the basolateral membrane domain of highly polarized intestinal absorptive cells was studied in adult rat intestinal mucosa, during development of polarity in fetal intestine, and in isolated epithelial sheets. Semi-thin frozen sections of these tissues were stained with a monoclonal antibody (mAb 4C4) directed against Na+,K+-ATPase, and with other reagents to visualize distributions of the membrane skeleton (fodrin), an epithelial cell adhesion molecule (uvomorulin), an apical membrane enzyme (aminopeptidase), and filamentous actin. In intact adult epithelium, Na+,K+-ATPase, membrane-associated fodrin, and uvomorulin were concentrated in the lateral, but not basal, subdomain. In the stratified epithelium of fetal intestine, both fodrin and uvomorulin were localized in areas of cell-cell contact at 16 and 17 d gestation, a stage when Na+,K+-ATPase was not yet expressed. These molecules were excluded from apical domains and from cell surfaces in contact with basal lamina. When Na+,K+-ATPase appeared at 18-19 d, it was codistributed with fodrin. Detachment of epithelial sheets from adult intestinal mucosa did not disrupt intercellular junctions or lateral cell contacts, but cytoplasmic blebs appeared at basal cell surfaces, and a diffuse pool of fodrin and actin accumulated in them. At the same time, Na+,K+-ATPase moved into the basal membrane subdomain, and extensive endocytosis of basolateral membrane, including Na+,K+-ATPase, occurred. Endocytosis of uvomorulin was not detected and no fodrin was associated with endocytic vesicles. Uvomorulin, along with some membrane-associated fodrin and some Na+,K+-ATPase, remained in the lateral membrane as long as intercellular contacts were maintained. Thus, in this polarized epithelium, interaction of lateral cell-cell adhesion molecules as well as basal cell-substrate interactions are required for maintaining the stability of the lateral membrane skeleton and the position of resident membrane proteins concentrated in the lateral membrane domain.

Aminopeptidases↗

PubMed2004

Pre-decondensed sperm head injections into female pronuclei result in chromosomal mingling, zygotic cleavage, and adequate embryonic and fetal development up to delivery of healthy offspring: a novel method of assisted syngamy.

Investigation of the developmental potential post-injection of a pre-decondensed or non-pre-decondensed sperm head into the female pronucleus of a pre-activated oocyte. Rat pre-activated oocytes were treated with intrapronuclear pre-decondensed sperm head injections (IPSHI) (n = 133) or intrapronuclear non-pre-decondensed sperm head injections (INPSHI) (n = 138). All injected oocytes were transferred to pseudopregnant female recipients. Rat IPSHI techniques resulted in the delivery of five healthy offspring. Rat INPSHI techniques did not result in any pregnancies. Rat IPSHI techniques can result in delivery of healthy offspring. Successful performance of human IPSHI techniques might serve as a novel method to manage cases of intracytoplasmic sperm injection failure due to lack of development of male pronucleus or due to failure in pronuclei fusion.

Animals↗

PubMed1982

Complications of pregnancy and fetal development.

Although the outcome of pregnancy for women with diabetes mellitus has improved in recent years, the infant of the diabetic mother has an increased risk of major clinical problems, particularly in the early neonatal period. These include birth injury due to macrosomia, neonatal hypoglycemia, respiratory distress syndrome, and serious congenital anomalies. Because of the great difficulties encountered during attempts to investigate these problems in clinical research protocols, there is a continuing need to establish appropriate animal models of the diabetic pregnancy. Studies carried out over the past decade, primarily with chemically-induced diabetes have suggested techniques which might be useful. In general, the choice of the animal to be studied will depend on the hypotheses being addressed. For instance, small animals such as rabbits and rats made diabetic with streptozotocin have been successfully used for investigation of fetal lung development. Furthermore, the rat model has been helpful for evaluation of fetal anomalies associated with maldevelopment of the spine and central nervous system. Larger animals, such as the nonhuman primate, are more appropriate for studying placental function and amniotic fluid composition in diabetic pregnancies. The task group on pregnancy and fetal development recommends that animal models of diabetes mellitus be used for a more extensive hormonal and metabolic characterization of diabetic mothers during pregnancy, for investigation of placental physiology with respect to the transfer of substrates from mother to fetus, for systematic and comprehensive study of mechanisms controlling fetal lung development, and for delineation of the pathophysiology of neonatal hypoglycemia. It is further recommended that animal models of spontaneous diabetes such as the BB/W rat be used in future studies dealing with pregnancy and fetal development. Because females with spontaneous diabetes show reduced conception rates, there is a pressing need to enhance the fertility of these animals in order to intensify studies on fetal development.

Alloxan↗

PubMed1985

The effect of maternal diabetes on trace element status and fetal development in the rat.

Despite improvements in prenatal care, there is a high incidence of congenital malformations in diabetic pregnancies. Not only is the diabetic patient characterized by a disorder of total fuel metabolism, but abnormal trace element metabolism occurs as well. In the present study, maternal and fetal zinc (Zn), copper (Cu), manganese (Mn), iron (Fe), magnesium (Mg), and calcium (Ca) status has been studied in Sprague-Dawley (SD) and Wistar rats. In addition, the effect of maternal diabetes on fetal development was also investigated. Rats were injected 27 days before mating with streptozocin (STZ, 45 mg/kg) in citrate buffer. On day 20 of gestation, litters were taken by cesarean section. Fetuses from diabetic dams weighed less, and had shorter crown-rump lengths and larger placentas than fetuses from controls. Evaluation of fetal skeletal development revealed fewer calcified sternal sites, anterior phalanges and caudal vertebrae, and an increased frequency of malformations in fetuses of diabetic dams. In dams, diabetics had larger adrenals, kidneys, and liver, and smaller thymus. Abnormal trace element metabolism was evident in diabetic dams and their fetuses. Mn was elevated in maternal liver, kidney and placenta of diabetic animals as well as in fetal liver of pups from diabetic dams. Maternal Cu and Zn levels were also higher in the liver and kidney of diabetic rats. In contrast, fetal liver Zn from fetuses of diabetic mothers was significantly decreased when compared with controls. These results suggest that diabetes may have induced fetal Zn deficiency. If this deficiency is present during embryogenesis/organogenesis, this could be one of the mechanisms of the teratogenicity of the diabetic state.

Animals↗

PubMed2005

Effects of feed restriction during organogenesis on embryo-fetal development in rabbit.

BACKGROUND: Appropriate maternal nutrition and body weight gain during pregnancy is well established as a major factor in healthy prenatal development in humans. Given the role of nutrition and body weight gain in normal development, pharmaceuticals intended to reduce appetite and promote weight loss will generate developmental toxicity data that may be challenging to interpret. To aid with this, the effects of feed restriction, and subsequent reduction in maternal body weight gain, on embryo-fetal development was investigated in the rabbit. METHODS: Groups of 15 pregnant New Zealand White rabbits were offered 150 (control), 110, 75, 55, 35, and 15 g feed/day from gestation day (GD) 7-19. Cesarean sections were carried out on GD 29 and fetuses were examined for external, visceral, and skeletal development. RESULTS: Maternal body weights at the end of the feed restriction period (GD 20) were 0.97, 0.98, 0.93, 0.94, and 0.86 x control for the 110, 75, 55, 35, and 15 g feed/day groups, respectively. Only at 15 g feed/day was there a net maternal body weight loss (the GD 20 body weight was 0.93 x the GD 6 body weight) at the end of the feed restriction period. Six does aborted in the 15 g feed/day group; there were no other abortions associated with feed restriction. Fetal body weight was significantly reduced at 75, 55, 35, and 15 g feed/day (0.95, 0.90, 0.86, and 0.84 x control, respectively). There were no external or visceral malformations or variations, and no skeletal malformations associated with feed restriction. The incidence of fetuses with sternebrae 5 or 6 unossified was increased at feed levels < or = 75 g/day. At a feed level of 35 g/day there was an increase in unossified metatarsals and metacarpals, and an increase in the number of fetuses with a reduced number of caudal vertebrae ossified. Although these findings were not increased at a feed level of 15 g/day, the lack of dose response was likely due to increased abortion and subsequent decrease in fetuses available for evaluation at 15 g feed/day. CONCLUSION: These data demonstrate that feed restriction to feed levels that produce substantial reductions in maternal body weight gain can result in developmental toxicity expressed by abortion, reduced fetal weight, and alterations in ossification. Abortion only occurred when feed was restricted to an amount that produced maternal body weight loss (15 g feed/day) whereas reduced fetal weight and increased incidence of fetuses with unossified sternebrae, metatarsals, metacarpals, or caudal vertebrae were noted at feed levels of < or = 75 g/day. There were no fetal malformations associated with feed restriction.

Animal Feed↗

PubMed1996

[The significance of psychosocial stress for pregnancy course and fetal development].

In a population-based study, 3021 women in a central Copenhagen district received a questionnaire on environmental and psychological factors during mid-gestation. Of these, 70 women were selected consecutively on the basis of moderate to severe stressful life-events (DSM-III-R categories 3 to 5), in combination with an inadequate social network. They were compared with 50 non-stressed women with an intact social network. Stress and smoking significantly affected birthweight and head circumference. When birthweight was corrected, stress remained a significant determinant of small head circumference, indicating a specific effect on brain development. Stress also led to a suboptimal Prechtl neonatal neurological score. These findings suggest the existence of a fetal stress syndrome with adverse effects on fetal development, including deficient brain development.

Birth Weight↗

PubMed2002

In vivo effect of leukemia inhibitory factor (LIF) and an anti-LIF polyclonal antibody on murine embryo and fetal development following exposure at the time of transcervical blastocyst transfer.

Leukemia inhibitory factor (LIF) enhances in vitro murine preimplantation development in a time- and dose-dependent fashion. Knockout experiments have demonstrated that endometrial LIF is essential for in vivo murine implantation. We assessed the impact of LIF and an anti-LIF polyclonal antibody (pab) on in vivo development and developed a novel and successful nonsurgical method of embryo transfer for this species, a transcervical blastocyst transfer technique. The objectives of this study were to evaluate the effects of LIF and the anti-LIF pab on 1) implantation, resorption, pregnancy, and viability rates and 2) the overall structural and skeletal development. Two-cell embryos were recovered from superovulated mated donors, cultured to the expanded blastocyst stage, and transferred transcervically into pseudopregnant recipients. Exposure to 5000 U/ml LIF resulted in significant increases in implantation, pregnancy, and viability rates compared with controls. A similar dose of pab produced overall inhibitory effects with a significant decrease in implantation rate. Paradoxically, lower pab doses resulted in significantly increased viability rates. Exposure to LIF had no effect on fetoplacental development. However, pab treatments had variable but significant negative effects on placental length, ossification of the exoccipital bone, and vertebral space width compared with controls. Exposure of murine blastocysts to LIF at the time of transcervical transfer resulted in pronounced positive effects on implantation and pregnancy rates without affecting fetal development. A similar pab dose dramatically reduced implantation and pregnancy rates; at high and low doses, pab produced deleterious effects on placental and skeletal development.

Animals↗

PubMed1988

Effects of N-acetylcysteine on fetal development and on phenytoin teratogenicity in mice.

The teratogenicity of phenytoin may result from its enzymatic bioactivation to a reactive intermediate, which interacts irreversibly with fetal tissues. Since glutathione (GSH) is involved in the detoxification of many reactive intermediates, N-acetylcysteine (NAC), a glutathione precursor, was evaluated for its effects on murine fetal development and phenytoin teratogenicity. NAC, 100 to 275 mg/kg, was given intraperitoneally (ip) or per os (po), or as 266 to 410 mg/kg in the drinking water, at various times before or after phenytoin, 65 to 75 mg/kg ip, on gestational days 12 and 13. Dams were killed on gestational day 19, fetal resorptions were noted, and fetuses were examined for anomalies. Significant reductions in phenytoin-induced fetal weight loss and cleft palates were observed when NAC was given by gavage 6 hours after phenytoin or in the drinking water with the lower dose of phenytoin. NAC administered in the drinking water also reduced the incidence of resorptions produced by the higher dose of phenytoin and enhanced postpartum survival in fetuses exposed to 65 or 75 mg/kg phenytoin (P less than .05). Conversely, the incidence of resorptions increased when NAC was given by gavage at other times before or after phenytoin, by single or repetitive ip injections, or in high concentrations in the drinking water (P less than .05). When given with the higher dose of phenytoin, NAC administered via the drinking water significantly increased the incidence of phenytoin-induced cleft palates and fetal weight loss (P less than .05). Similar results were obtained with a single ip injection of NAC and a lower dose of phenytoin. Thus, when given orally, NAC can partially reduce phenytoin teratogenicity and embryopathy. However, altering the route of NAC administration, or increasing the dose of phenytoin and/or NAC, enhanced phenytoin embryotoxicity, and NAC alone at higher doses had embryopathic effects.

Acetylcysteine↗

PubMed1995

Effect of diethylstilbestrol or zeranol on fetal development, gestation duration, and number of offspring in NMRI mice.

OBJECTIVE: To evaluate the effects of diethylstilbestrol (DES) or alpha-zearalanol (zeranol) on fetal development, gestation duration, and number of offspring. DESIGN: Study effects of prenatal administration of DES or zeranol on various pre- and perinatal variables in an experimental group of mice, compared with effects in a control group. ANIMALS: Pregnant NMRI mice. PROCEDURE: Diethylstilbestrol or zeranol (150 mg/kg of body weight) or vehicle (controls) was administered SC to pregnant mice on days 9 and 10 of gestation. Fetuses from pregnant mice of each group were counted and weighed, and their size and head length were recorded. Additional pregnant mice delivered their fetuses naturally, and pups from each group were counted and their sex was determined. At the end of gestation, abortions were evaluated. All data were statistically analyzed. RESULTS: Mean number of fetuses was significantly lower (P < 0.0001) in DES-treated (4.59 +/- 0.48) than in control mice (8.33 +/- 0.49). Both estrogenic substances significantly reduced fetal size and weight (P < 0.0001), compared with control mice. Diethylstilbestrol significantly increased abortion frequency (P < 0.0001) and gestation duration (P < 0.0001), compared with values for control mice. A reduced number of live pups (P < 0.0001) from pregnant mice administered DES (5.48 +/- 0.38) or zeranol (5.97 +/- 0.49) was observed, compared with control mice (8.52 +/- 0.50), because of reduced number of male offspring (P < 0.0001). CONCLUSIONS: Diethylstilbestrol or zeranol administered during mid-pregnancy leads to decreased fetal weight and size and lower numbers of male offspring at birth. Likewise, DES induced a significant increase in abortions and gestation duration.

Animals↗

PubMed1998

Fetal development of the pituitary gland in the beagle.

BACKGROUND: The pituitary gland of the dog is different from all animals and is described as "typical" for mammals. How might this complex pituitary gland of the dog be formed in fetal life? The current study examined the fetal development of the complex and unique dog pituitary and the ontogeny of specific cell types in the pars distalis. METHODS: Adenohypophysis of the beagle, from 25 to 60 days of gestation and at 2 days of age, was studied by immunocytochemical and histological staining. RESULTS: At 25 days gestation, the primordium (Rathke's pouch) of the adenohypophysis began to form by an upward evagination from the epithelium of the primary oral cavity. At 38 days, the pituitary gland showed the same morphology as in adult dogs, being merely smaller. Five walls of Rathke's pouch (anterior wall [A], lateral walls [L], posterior wall [P], and upper wall [U] were found at 25 days, and by 38 days they had specialized into specific regions of the adenohypophysis through complex and unique processes. The pars intermedia was derived from the U and the dorsal area of the A. The pars tuberalis was derived from the dorsal area of the A. The pars distalis was formed by more singular processes: the peripheral areas of the pars distalis were first formed by A and P; then the ventral lumen of the extensive Rathke's lumen surrounded by these areas was filled up by proliferation of cells, although the dorsal lumen remains as Rathke's lumen after 38 days. The blood capillaries may play an important role in the development of parencymal cells in the Rathke's pouch during canine fetal life. At 30 days gestation, the first adrenocorticotropic hormone cells were found in the anterior- and posterior-ventral regions (derived from middle and ventral areas of the A and the P) of the pars distalis anlage, and blood capillaries invaded the parenchymal cells from the mesencyme surrounding the anlage. At 38 days, portal vessels without capillary loops in the median eminence had appeared, and growth hormone and luteinizing hormone cells appeared in the ventral areas of A and P in the pars distalis. By 52 days, when capillary loops were seen in the portal vessels in the median eminence, these types of cells spread through the whole pars distalis. CONCLUSION: These areas in the epithelium of Rathke's pouch at 25 days may differentiate into specific regions of the pars distalis during subsequent fetal life, through complex processes that are characteristics to the canine species.

Adrenal Glands↗

PubMed1992

Pathological effects of maternal hypoglycemia on fetal development in cats.

The pathogenesis of fetal brain damage caused by acute maternal hypoglycemia was investigated experimentally in cats: profound hypoglycemia (blood glucose concentration: less than 30 mg/dl) was induced in 12 pregnant cats at various stages of gestation by intravenous bolus injections of insulin. Maximal hypoglycemia was attained within 2-3 h, although the grade and duration in individual cats varied. The EEGs of all of seven maternal cats examined showed an increased frequency of slow high-voltage waves as hypoglycemia progressed, eventually becoming flat in 3 for a maximum period of 20 min. Some fetuses showed severe neuropathological changes, such as infarction or intrauterine death. Subventricular softening, cortical hemorrhage and ischemic neuronal changes also occurred, being distributed symmetrically in the parasagittal areas of the cerebrum, basal ganglia, thalamus and tegmentum of the brainstem. In general, these pathological changes were more marked in fetuses and neonates than in the maternal cats, in which only ischemic neuronal changes were present, and may have been due to fetal systemic hypotension and cerebral ischemia induced by hypoglycemia. In maternal cats, the distribution of neurons showing ischemic changes was widest in the cerebral cortex, and some were also present in the dentate gyri of the hippocampus. Moreover, ultrastructural examination of the ischemic neurons in maternal cats, unlike those of the fetuses, showed no mitochondrial swelling. Therefore, the distribution and ultrastructural nature of the ischemic neurons found in the maternal cats were considered to be characteristic of hypoglycemia, as proposed by Agardh et al. (1980).

Animals↗