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Biomedical subjects

A B Lansdown

Publications and source records attributed to A B Lansdown.

At least 37 records · Page 2Linked to original sources
PubMed1978

Pathological observations on experimental cytomegalovirus infections in pregnancy.

Cytomegalovirus injected intramuscularly or intraperitoneally into mice on the 8th day of pregnancy resulted in a significant retardation in foetal growth and a reduced number of offspring surviving until near-term. Pathological changes consisted of inflammatory cell infiltration in the liver, heart, salivary glands and adrenal cortex of affected animals. Necrotic changes were also present in the adrenal cortex in most severely affected animals following intraperitoneal injection of virus. Intraperitoneal infection led to a frank peritonitis and marked splenic necrosis with a degeneration and inflammation of visceral fatty tissue and lymphadenitis. In contrast, intramuscular injection of virus did not produce a peritonitis but the spleen was greatly enlarged with reaction centres and increased numbers of lymphocytes being identified at histology. As a consequence of cytomegalovirus infection in pregnant mice foetal growth impairment and intrauterine death was seen. This was related to the severity of pathological changes in the mothers. In those animals dying or appearing sick at near-term, most foetuses were dead and resorbing. Since murine cytomegalovirus was not identified by inclusion body formation in foetal or placental tissues in this study and virus has not been isolated from these tissues previously, it was concluded that the mechanism for the impaired foetal growth was of an indirect nature and attributable primarily to a severe generalised maternal illness.

Animals↗
PubMed1978

Fetotoxicity in rats following chronic exposure to halothane, nitrous oxide, or methoxyflurane.

An animal model was used to investigate the comparative fetal toxicities of three inhalational anesthetics. Pregnant Sprague-Dawley rats were exposed for eight hours a day throughout the 21 days of gestation to graded concentrations of halothane (0.16-0.32 per cent), or nitrous oxide (1-50 per cent), or a nitrous oxide (10 per cent) and halothane (0.16 per cent) mixture, or methoxyflurane (0.01-0.08 per cent). High subanesthetic concentrations of all the inhalational anesthetics could cause fetal growth retardation (e.g., 3-21 per cent decreases in normal fetal weights), but this was unaccompanied by significant fetal loss (overall rate: 4.8 +/- 1.2 per cent, mean +/- SE, in anesthetic groups) or any evidence of skeletal or gross abnormalities related to treatment. It is concluded that these rodent studies do not implicate any specific inhalational anesthetic agent in fetal toxicity, and that the effects of additional factors, such as stress, must be considered.

Animals↗
PubMed1978

Epidermal differentiation in normal and growth-retarded infants: studies in two animal models and in human babies.

The influence of prenatal growth retardation on epidermal growth and keratinization was studied in small-for-dates human babies, runt piglets and in rat fetuses subject to maternal protein deprivation. In the human babies and rat fetuses growth retardation was associated with reduced epidermal growth but normal patterns of differentiation were present. Thus, epidermal thickness was less and keratinizing zones narrower than seen in normal weight individuals. In the runt (small-for-dates) piglet, epidermal development differed from that seen in normal weight piglets of the same gestational age and from that seen in the human and rat. The epidermis was thicker with a negligible stratum granulosum and with the stratum corneum containing nucleated cells, a condition resembling 'parakeratosis'. This pattern was less often seen in normal weight piglets. Differences between the skins of the three speecies studied at a perinatal stage may be related to clear dissimilarities which exist in the tissues later. Parakeratosis as a transitory phase in the development of pig skin is probably related to a higher rate of epidermal keratinization in this species than occurs in either human babies or rat fetuses.

Animals↗
PubMed1977

Histological observations on thymic development in fetal and newborn mammals subject to intrauterine growth retardation.

Fetal growth retardation resulting from maternal dietary protein deprivation (rats) or Coxsackie virus B3 infection in mid-pregnancy (mice) was associated with delayed thymic development. Histological examination revealed that less darkly staining small lymphocytes were present and that the thymus was not well organised into cortex and medulla as seen in the normal-weight fetuses. In preterm or neonatal piglets, the histological pattern of the thymus did not vary appreciably according to the body weight of the fetus. Hassall's corpuscles were present and the tissues were well organised into cortex and medulla regions. Although fetal growth retardation in rats and mice leads to an apparent delay in the differentiation of the thymus, functional studies are necessary to understand the immunological significance of this finding.

Animals↗
PubMed1977

Coxsackievirus B3 infection in pregnancy and its influence on foetal heart development.

Infection of mice on the 12th or 14th day of pregnancy with Coxsackievirus B3 resulted in the birth of growth-retarded young which died soon after birth and exhibited an abnormal heart development. The ratio of heart weight to body weight in these offspring was higher than normal. The auricles were prominent and the ventricles developed such that the heart apex was bifid in appearance. This anomalous cardiac development may have been due to a direct viral pathogenicity in the developing tissue or, as seems more likely, resulted from a generalized disturbance in foetal growth attributable to a virus-induced pancreatic insufficiency in the mother. Retarded development in the pulmonary system also resulting from aberrations in foetal growth may have been contributory to impaired postnatal cardiac growth.

Animals↗
PubMed1976

Pathological changes in the pancreas of mice following infection with Coxsackie B viruses.

Infection of pregnant or non-pregnant mice with Coxsackieviruses B1, B3, B4 or B5 produced a severe pancreatitis consisting of a degeneration of the acinar cells, loss of zymogen granules, infiltration of mononuclear and plasma cells and a replacement of the exocrine tissue with fatty tissue. Coxsackieviruses B2 and B6 did not cause these changes in the period up to 6 weeks following virus injection. Suckling mice did not appear to be more susceptible to pancreatic damage due to these two viruses. Sequential studies on the development of Coxsackievirus B-induced pancreatic lesions indicated that although the changes due to B1, B3, B4 or B5 were similar in type, B3 and B4 exhibited a more rapid action in the tissue and more severe lesions than either B1 or B5. In this work, none of the Coxsackie B viruses examined elicited pathological changes in the islets of Langerhans detectable with the light microscope.

Animals↗
PubMed1976

Immunization of mice against Coxsackievirus B3 and prevention of foetal growth retardation.

Coxsackievirus B3 infection in pregnant mice leads to a severe pancreatitis with a retardation of foetal growth and increased wastage. The present study demonstrates that animals may be immunized actively or passively against this infection to allow foetal development to proceed normally. Active immunization was achieved by injecting a low dose of live virus into 4-week-old animals. These mice were then mated at 10 weeks and given a high dose of virus on the eighth day of pregnancy. Examination at 18 days' gestation revealed that foetal growth was not significantly different from the controls injected with heat-killed virus, and pathological changes in the mothers were not seen. Animals were passively immunized against Coxsackievirus B3 in pregnancy by injecting serum from immunized animals 1 day before the high dose of live virus was given. This procedure also protected against the effects of the virus and litter sizes and foetal weights were normal.

Animals↗
PubMed1975

Histological observations on epidermal development in fetal mice subject to intrauterine growth retardation due to maternal infections with Coxsackievirus B3.

Infection of mice with Coxsackievirus B3 on the 8th day of pregnancy resulted in fetal growth retardation. A histological examination of interscapular back skin of infected fetuses revealed an immature pattern of differentiation at 18 days gestation with the epidermis being appreciably thinner than normal, but equivalent to that of a 15-day fetus. The pattern of keratinization as demonstrated by fluorescence microscopy, and the deposition of epidermal phospholipid were normal in these retarded fetuses but less well developed. Retarded keratinization in the infected fetuses was related to abnormal amniotic fluid compositions due to reduced maternal health resulting from virus-induced pancreatic exocrine insufficiency.

Amniotic Fluid↗
PubMed1975

Influence of time of infection during pregnancy with coxsackievirus B3 on maternal pathology and foetal growth in mice.

Coxsackievirus B3 causes foetal wastage and growth retardation in mice which may be attributed to the action of the virus in destroying the maternal exocrine pancreas. Injection of virus on Day 4 or 8 of gestation caused greater foetal wastage than injection at 12 days. Foetal and placental weights in infected animals were less than in the controls but did not vary according to the time of infection. Little support is offered for the view that the mouse foetus differs in its susceptibility to Coxsackievirus B3 according to the stage in gestation of infection.

Animals↗
PubMed1975

Pathological changes in pregnant mice infected with Coxsackievirus B3 and given dietary casein hydrolysate supplement.

Coxsackievirus B3 infection in pregnant mice leads to a severe pancreatic exocrine insufficiency in the mothers and retarded foetal growth. As a consequence of the pancreatic damage, the animals are rendered incapable of digesting sufficient amounts of dietary proteins to allow maternal liver development to proceed as normal for the pregnant rodent. Faecal nitrogen was increased and the maternal livers were small for the weights of the animals and exhibited a lower than normal nitrogen content. Feeding of additional amino acids and simple peptides in the diet in the form of casein hydrolysate either from before or after virus injection appeared to compensate for the inability of these animals to digest dietary protein nitrogen and allowed maternal liver development and foetal growth to proceed at a rate not significantly different from normal. Although these results apply to infections with Coxsackievirus B3 in pregnancy, they may be relevant to other infections which adversely affect foetal growth by their pathological effects on maternal organs necessary for maintaining optimal foetal growth.

Animals↗
PubMed1975

Lack of teratogenic dangers with halothane.

Chronic exposure of pregnant Sprague Dawley rats to a range of halothane concentrations from 50-3200 p.p.m. for 8 hours a day on days 8-12 of gestation failed to demonstrate significant teratogenicity in terms of foetal loss, growth, or skeletal abnormalities. Exposure to 1600 p.p.m. showed significant changes only in foetal weights, which were slightly decreased.

Abnormalities, Drug-Induced↗