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Biomedical subjects

T V Persaud

Publications and source records attributed to T V Persaud.

At least 73 records · Page 4Linked to original sources
PubMed1982

Protection against ethanol-induced embryonic damage by administering gamma-linolenic and linoleic acids.

Many reports have now confirmed the teratogenic potential of alcohol in humans and in laboratory animals. A characteristic pattern of congenital anomalies is present in infants born to mothers suffering from chronic alcoholism. The pathogenesis of this condition is unclear. Chronic consumption of ethanol causes a depletion of essential fatty acids, partly by blocking gamma-linolenic acid formation and partly by depleting dihomogammalinolenic acid. Whether this action of ethanol on essential fatty acid and prostaglandin metabolism may account for its teratogenic potential was investigated in the rat. Treatment of pregnant rats with ethanol and evening primrose oil (efamol), a rich source of gammalinolenic acid, led to a significant reduction in the embryopathic activity of ethanol.

Animals↗
PubMed1982

Further studies on the interaction of ethanol and nicotine in the pregnant rat.

Because alcohol and cigarette smoking are considered to be deleterious to the fetus, the combined effect of ethanol and nicotine during pregnancy was investigated. Pregnant Sprague-Dawley rats receiving a liquid alcohol diet at moderate dose-levels from gestational day 1 through 12, and a continuous subcutaneous infusion of nicotine from gestational day 6 through 12, revealed no significant reproductive and developmental disturbances.

Animals↗
PubMed1981

Prostaglandin F2alpha conceptus-endometrial interaction during early gestation in the mouse.

Pregnant Swiss-Webster mice were treated subcutaneously with 50, 100 or 200 microgram PGF2alpha on day 4, 5 or 6 postcoitum (p.c.). Twelve hours later, the animals were killed by intracardiac perfusion with Karnovsky's fixative, uteri were removed and a transverse central slice from each implantation site was embedded in Araldite. The conceptus was found by thick sectioning. Thin sections were taken of each implantation site and examined at the electron microscopic level. PGF2alpha administered at a dose of 100 microgram per animal on day 4 p.c. altered the normal attachment of the blastocyst to the endometrium, as well as formation of the implantation chamber. Cytology of the epiblast and hypoblast was adversely affected by this change. Dosages of 100 or 200 microgram PGF2alpha per animal adversely affected the apical trophectoderm cell of the blastocyst. Treatment with PGF2alpha on day 4 p.c. at a dose of 50 microgram per animal reduced the decidual reaction around the implantation chamber while treatment on day 5 p.c. at a dose of 50 or 100 microgram per animal was associated with an advanced stage of development. Treatment on day 6 p.c. did not appear to have any influence on implantation or blastocyst development.

Animals↗
PubMed1981

Development of the chick embryo following PGE1 treatment.

Chick embryos were treated with prostaglandin E1 (10, 20, 30, and 50 micrograms) at 48 and 72 hours incubation. Live embryos were recovered on day 9, staged, and examined for external malformations after weighing. There was no significant increase in embryonic mortality and malformation rates compared to the controls. Embryonic growth was also not affected.

Animals↗
PubMed1981

Embryopathic effects of thromboxane B2 in the chick.

Several prostaglandins of the E and F series are now known to be involved in reproduction and developmental events. However, there is as yet no such evidence for any of the other arachidonate metabolites. Thromboxane B2 is the stable metabolic end product of the biologically active but unstable intermediate thromboxane A. Administered to developing chick embryos at 48 and 72 hours incubation, thromboxane B2 caused growth retardation and induced a high incidence of anomalies, in particular, everted viscera.

Animals↗
PubMed1981

Abnormal development of the central nervous system.

Abnormal development of the neural tube occurs with a high frequency and produces a wide range of malformations of the brain and spinal cord. Most dysraphic conditions are severe and, with the exception of meningomyelocele, lead to early death. This review deals with the more common clinically important neural malformations from the standpoint of epidemiology, etiology and pathogenesis based on both clinical and experimental observations.

Anencephaly↗
PubMed1981

Prostaglandin F2 alpha effects on the early mouse embryo.

Subcutaneous treatment of pregnant mice with 50, 100 and 200 micrograms PGF 2 alpha on gestational day 5 and 200 micrograms on gestational day 3 or 6 resulted in fetal growth retardation. Litter size was significantly reduced following treatment with 50 micrograms or 100 micrograms PGF 2 alpha on day 6 of pregnancy and the incidence of resorptions was increased following treatment with 50 micrograms on gestational day 6.

Animals↗
PubMed1980

Distribution of prostaglandin F1 alpha in the pregnant rat.

The placental transfer and tissue distribution of tritium-labelled prostaglandin F1 alpha was investigated in rats on day 14 of gestation. Low levels of radioactivity were detected in the embryos and placentas 5, 10, 60, and 120 minutes after administration of the prostaglandin, but the concentration in amniotic fluid was extremely high at all time intervals. Maternal serum, kidney, liver and lung revealed a greater uptake of the isotope compared to the uterus, ovary, spleen and brain. It is conceivable that the high levels of prostaglandin accumulated in the amniotic fluid may act directly on the conceptus.

Amniotic Fluid↗
PubMed1980

Pregnancy and progeny in rats treated with prostaglandin F1 alpha.

Studies on the influence of PGF1 alpha on reproductive processes in humans and laboratory animals are lacking. PGF1 alpha was administered s.c. to pregnant Sprague-Dawley rats at doses of 50, 100, and 200 micrograms, respectively, from days 12 through 15 of gestation. The offspring, recovered by cesarean section on gestational day 20, were all alive and showed no anomalies. The incidence of fetal resorptions was not significantly increased. However, PGF1 alpha caused intrauterine growth retardation and placental damage. There was no morphological evidence of luteolysis.

Animals↗
PubMed1980

Compensatory embryonic development in the rat following maternal treatment with ethanol.

A pattern of congenital anomalies, termed "fetal alcohol syndrome", has been recognized in the offspring of mothers with chronic alcoholism. The teratogenic mechanism is not known. Moderate doses of ethanol, administered to pregnant rats from day 5 through 8 of gestation, impaired blastocyst development. The mean fetal weight on day 20 of gestation was reducted, compared to that of the controls. However, fetal survival was not affected and congenital anomalies were not detected in any of the offspring. These results indicate that considerable compensatory growth and repair may obscure early embryopathic lesions before development is completed.

Animals↗
PubMed1980

Effect of ethanol and nicotine in the pregnant rat.

Treatment of pregnant Sprague-Dawley rats on day 9 of gestation with both ethanol (0.02 ml/gm of a 12.5% or 25% solution, i.p.) and nicotine (5 mg/kg, s.c.) resulted in no significant adverse effects on embryonic development and fetal viability.

Abnormalities, Drug-Induced↗
PubMed1979

Morphology of experimental spina bifida in the chick embryo.

Open malformations of the central nervous system may involve the brain or spinal cord, or both. Preliminary experiments in which a window was cut in the shell overlying early chick embryos (with removal of 2 ml of albumen) produced a range of neural and non-neural malformations. Exposure of Stage 5--10 embryos at 26 hours of incubation produced open brain and cord defects. Embryos were recovered at 11--12 days for gross examination. Open cord defects in 12 day experimental embryos could be divided morphologically into 2 types. One group showed an everted symmetrical plaque of neural tissue. In the other group the cord defect was more irregular, partly covered by skin, and often combined with rump and trunk defects. Skeletal staining showed that vertebral lesions increased in severity in a cranio-caudal sequence. Spina bifida occulta was found in the cervical and upper thoracic regions; spina bifida manifesta, associated with open cord defects, occurred from the lower thoracic to the sacral regions; vertebral deletions were almost confined to the caudal region. Spina bifida manifesta at the site of open cord defects also showed 2 distinct patterns. Regular cord defects were associated with regular spinal defects, showing loss of spinous processes, reduction of laminae and eversion of the pedicles. Irregular cord defects were associated with more irregular spinal defects showing vertebral deletions or fusions, rumplessness, and pelvic reduction. Neither group, however, showed local kyphosis or scoliosis. Early neurogenesis in the avian and human embryos is very similar with development of the spinal cord from neural plate and tail bud materials which fuse in an overlap zone. These experimental defects in the chick embryo, separable into regular and irregular types thus provide a useful model for investigation of the embryogenesis of spina bifida.

Abnormalities, Multiple↗
PubMed1979

Histogenesis of experimental open neural defects in the early chick embryo.

The chick embryo is a useful experimental model for investigating neural dysraphism. Windowing at 26 h incubation is by itself teratogenic, resulting in predominantly neural tube defects. A histological study of a regular series of specimens between pre-neurulation and later stages was undertaken. Open brain defects occurred at every stage after the expected closure of the anterior neuropore, suggesting that they arose by non-closure, myeloschisis was preceded by a characteristic triangular shape of the rhomboid sinus. Serial sections revealed regular open defects, with separation between the neural plate and tail-bud sources of neural tissue, but continuity of the neural plate into the caudal region. These findings suggest that myeloschisis arises by nonclosure of the neural folds. The establishment of myeloschisis was followed by local separation of the notochord from an open area of neural tube, but not by overgrowth of neural tissue. Myelodysplasia appeared at about the time of expected closure of the rhomboid sinus. Serial sections revealed irregular open defects, with complete absence of neural plate material and formation of the cord tissue from tailbud material alone. The lesions were accompanied by extensive cystic and hemorrhagic changes in local mesoderm, with reduction in somite volume. There was no associated notochordal separation.

Animals↗