Effect of inhibiting prostaglandin synthesis in pregnant sheep with 4-aminoantipyrine under normothermic and hyperthermic conditions

Andrianakis, P.; Walker, David W.; Ralph, M. M.; Thorburn, G. D.

doi:10.1016/0002-9378(89)90273-1

Cited by 21 publications

(15 citation statements)

References 22 publications

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“…The fetus was then removed from the uterus through a 6-10 cm incision taking care not to stretch or damage the umbilical cord. The fetus and uterus were covered by a large plastic bag to prevent loss of moisture and heat by evaporation, and also wrapped in the heating blanket and towelling to maintain the fetal temperature, monitored with a probe in the rectum, at 38-39°C, which is in the range of normal fetal temperatures (Andrianakis, Walker, Ralph & Thorburn, 1989). The right fetal hindlimb was extended and the soleus, MG and FDL muscles were dissected free of surrounding tissues, taking care not to damage the blood and nerve supplies.…”

Section: Methodsmentioning

confidence: 99%

Growth and differentiation of fast and slow muscles in fetal sheep, and the effects of hypophysectomy.

Javen

Williams

Young

et al. 1996

The Journal of Physiology

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Section: Methodsmentioning

confidence: 99%

Growth and differentiation of fast and slow muscles in fetal sheep, and the effects of hypophysectomy.

Javen

Williams

Young

et al. 1996

The Journal of Physiology

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“…Since this kind of change is well correlated to a reduction in thyroid hormone secretion rate in the adult, the results suggest that the thyroid gland participates in active neuroen docrine regulation of heat production in the fetus. Previous studies have shown that the fetus is warmer than the mother by 0.5-1.0 °C and that the fetal-maternal tempera ture gradient is maintained during maternal hyperthermia induced by external heating [17][18][19][20]. It is therefore likely that fetal tem peratures in the vicinity of 41 °C were present in the heat-stressed ewes.…”

Section: Discussionmentioning

confidence: 99%

“…The difference in rectal tempera ture between the two groups was significant (unpaired t = 7.69, df = 18; p < 0.01). Since the normal fetomaternal temperature differ ence is maintained over a range of maternal temperatures [17][18][19], fetal temperature would probably be 0.6-1.0 °C above both the normal and hyperthermic maternal val ues and would therefore have reached 41 °C in the heated group [19], Fetal temperatures were not measured at autopsy, since the measurements would not accurately reflect fetal temperatures in utero.…”

Section: Emperaturesmentioning

confidence: 99%

Effect of Hyperthermia on Thyroid Structure in the Late Gestation Fetal Lamb

Andrianakis

Stephenson²,

Walker³

1990

Neonatology

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This study examined the effect of hyperthermia in late gestation on fetal thyroid structure. Mild heat stress (increase of ewe’s rectal temperature to 40.4°C) caused significant changes of fetal thyroid structure. Intra-follicular colloid area was significantly larger in the heat-stressed group (2,532 ± 181 μm²) compared to a control group where rectal temperature of the ewe was within the normal range (1,660 ± 188 μm²; p < 0.01). Epithelial cell height was significantly reduced (2.5 ± 0.19 vs. 4.8 ± 0.26 μm; p < 0.01). Fetal plasma glucose concentrations were significantly lower in the heat-stressed group (0.7 ± 0.07 mmol/l) compared to the non-heated group (1.0 ± 0.11 mmol/l; p < 0.05). We suggest that the fetal thyroid gland in sheep is responsive to environmental temperature changes and is important in the neuroendocrine regulation of fetal body temperature. Fetal hypoglycaemia may also contribute to the changes in fetal thyroid gland by altering the peripheral utilization of thyroid hormone. Such changes, if prolonged, may contribute to the decreased rate of fetal growth and maturation associated with chronic heat stress in sheep.

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“…It is notable that abortion is a common sequel to a febrile episode (Kline et al, 1985) and it is probable that this is the outcome in most instances of maternal heat exposure . Hyperthermia is associated with an increase in the plasma levels of prostaglandins (PGs) in the ewe and fetal lamb (Andrianakis et al, 1989) and is accompanied by increased uterine activity and fetal distress (Morishima et al ., 1975). There are many reports of retrospective and prospective studies on the occurrence of NTD after maternal exposures to a range of conditions leading to elevations of temperature (Chance and Smith, 1978;Layde et al, 1980;Shiota, 1982;Hunter, 1984;Milunsky et al ., 1992) and it has been estimated that maternal hyperthermia at the time of neural tube closure is the cause of about 10% of cases of NTD .…”

Section: Developmental Defects Caused By Hyperthermiamentioning

confidence: 99%

“…Andrianakis et al (1989) exposed pregnant sheep to a hot environment which elevated the maternal and fetal temperatures and caused elevation of prostaglandin (PG) plasma levels in the mother and fetus. Inhibition of PG synthesis caused fetal distress and at times, fetal death.…”

Section: Signal Transduction Pathwaysmentioning

confidence: 99%

Heat shock proteins and their role in early mammalian development

Walsh

Mj²,

Smith³

1997

Exp Mol Med

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A b s t r a c tElevated body temperature can result from many agents in the natural environment, such as fever, hot weather and heavy exercise. In our modern living conditions additional sources of induced hyperthermia including hot baths, saunas, drugs, electromagnetic radiation and ultrasound have been introduced. Hyperthermia during pregnancy has been shown to cause a wide spectrun of effects in all species studied, including humans, the outcome depending on the dose of heat absorbed by the mother and embryo and the stage of enbryonic or fetal development when exposed. The dose of heat is the product of the elevation of temperature above normal and the duration of the elevation. In relatively uncontrolled natural environmental exposures, embryonic death and resorption or abortion are probably the most common outcome. In less severe exposures (smaller doses) major or minor developmental defects can result and the central nervous system appears to be a major target for its effects. Heat damage to embryos appears to be by apoptotic and other forms of cell death in organs at critical stages of development. Over many millennia all living orgaisms appear to have developed protective m e c h a n i s m s against excess heat, known collectively as the heat shock response. This response has been s t u d i e d intensively over the last 20 years and its mechanisms of protection are now becoming more clearly defined. Exposures to heat (and a number of other toxic agents) trigger the heat shock response which is characterized by abrupt suspension in the normal protein synthesis and the concurrent induction of heat shock genes (hsp) and the synthesis of a set of protein families known collectively as the heat shock proteins (HSP). The hsp are known to be involved in the response in embryos, each has at least two copies, one which appears to have functions in the normal embryonic development (cognate) and another which is induced at a certain dose of heat (induced) and which can offer some protection against damage for some time after the initiating dose.

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Effect of inhibiting prostaglandin synthesis in pregnant sheep with 4-aminoantipyrine under normothermic and hyperthermic conditions

Cited by 21 publications

References 22 publications

Growth and differentiation of fast and slow muscles in fetal sheep, and the effects of hypophysectomy.

Growth and differentiation of fast and slow muscles in fetal sheep, and the effects of hypophysectomy.

Effect of Hyperthermia on Thyroid Structure in the Late Gestation Fetal Lamb

Heat shock proteins and their role in early mammalian development

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