Hostname: page-component-586b7cd67f-r5fsc Total loading time: 0 Render date: 2024-11-24T15:05:00.353Z Has data issue: false hasContentIssue false
  • English
  • Français

Visceroatrial heterotaxy syndrome induced by maternal hyperthermia in the rat

Published online by Cambridge University Press:  19 August 2008

Masae Morishima ,
Sachiko Miyagawa-Tomita ,
Hiroshi Yasui ,
Masahiko Ando ,
Makoto Nakazawa  and
Atsuyoshi Takao
Sachiko Miyagawa-Tomita
Affiliation:
From the Research Division and Department of Pediatric Cardiology, Tokyo Women's Medical College, Tokyo
Hiroshi Yasui
Affiliation:
The Heart Institute of Japan, Department of Anatomy and Developmental Biology, Tokyo Women's Medical College, Tokyo
Masahiko Ando
Affiliation:
From the Research Division and Department of Pediatric Cardiology, Tokyo Women's Medical College, Tokyo
Makoto Nakazawa
Affiliation:
From the Research Division and Department of Pediatric Cardiology, Tokyo Women's Medical College, Tokyo
Atsuyoshi Takao
Affiliation:
International Center for Molecular, Cellular and Immunological Research, Tokyo Women's Medical College, Tokyo
Get access Rights & Permissions [Opens in a new window]

Summary

Maternal hyperthermia induces malformations in human and laboratory animals, but there are only a few reports of cardiovascular anomalies induced by maternal hyperthermia. Pregnant Wistar Imamichi rats were exposed to hyperthermia on day nine of gestation by immersion in a hot-water bath (43.0–43.5 °C) twice a day. Their fetuses were examined on day 18 after fixing with 2.5% glutaraldehyde solution. According to the average body temperature of the dam, the fetuses were divided into five groups, each group increasing by 0.1 °C from 42.5 °C to 42.9 °C. The incidence of cardiovascular anomalies was increased from 24 to 100% with the rise in body temperature of the dams. In the groups with average temperatures of 42.8 and 42.9 °C, most of the fetuses (70–80% of cases with anomalies) showed visceroatrial heterotaxy associated with severe cardiovascular anomalies, including common atrioventricular orifices with double outlet right ventricle or discordant ventriculo-arterial connections. The visceral structures of those fetuses showed a tendency to left isomerism, such as bilateral left atrial appendages, single lobation of the lung on both sides, a symmetrical liver with interruption of the posterior caval vein, hypoplasia of the spleen, and malrotation of the intestinal loop. Day nine of gestation in the rat may be a critical period for determining left-right sidedness of the viscera. The results indicate that the determination of morphological left-sidedness of visceral structures is related in some way with maternal hyperthermia.

Keywords

Maternal hyperthermiacardiovascular anomaliesvisceroatrial arrangementleft isomerismheterotaxy
Type
Original Manuscripts
Information
Cardiology in the Young , Volume 5 , Issue 3 , July 1995 , pp. 251 - 256
Copyright
Copyright © Cambridge University Press 1995

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Fisher, NL, Smith, DW. Occipital encephalocele and early gestational hyperthermia. Pediatrics 1981; 68: 480–483.CrossRefGoogle ScholarPubMed
2.Smith, MSR, Upfold, JB, Edwards, MJ, Shiota, K, Cawdell-Smith, J. The induction of neural tube defects by maternal hyperthermia: a comparison of the guinea pig and human. Neuropathol Appl Neurobiol 1992; 18: 71–80.CrossRefGoogle ScholarPubMed
3.Edwards, MJ. Congenital malformations in the rat following induced hyperthermia during gestation. Teratology 1968; 1: 173–175.CrossRefGoogle ScholarPubMed
4.Webster, WS, Edwards, MJ. Hyperthermia and the induction of the neural tube defects in mice. Teratology 1984; 29: 417–425.CrossRefGoogle ScholarPubMed
5.Webster, WS, Germain, MA, Edwards, MJ. The induction of microphthalmia, encephalocele, and other head defects following hyperthermia during the gastrulation process in the rat. Teratology 1985: 31: 73–82.CrossRefGoogle ScholarPubMed
6.Nakazawa, M, Miyagawa, ST, Morishima, M, Kajio, F, Takao, A. Effects of environmental hyperthermia on cardiovascular function in the rat embryo. Ped Res 1991; 30: 505–508.CrossRefGoogle ScholarPubMed
7.Clark, EB. In: Pierpont, MEM, Moller, JH (eds). The Genetics of Cardiovascular Disease. Martinus Nijhoff Publishing, 1987, pp 3–11.CrossRefGoogle Scholar
8.Miyagawa, S, Kirby, ML. Pathogenesis of persistent truncus arteriosus induced by nimustine hydrochloride in chick embryos. Teratology 1989; 39: 287–294.CrossRefGoogle ScholarPubMed
9.Hummel, KP, Chapman, DB. Visceral inversion and associated anomalies in the mouse. J Hered 1959; 50: 9–13.CrossRefGoogle Scholar
10.Brueckner, M, D'Eustachio, P, Horwich, AL. Linkage mapping of a mouse gene, iv, that controls left-right asymmetry of the heart and viscera. Proc Natl Acad Sci USA 1989; 86: 5035–5038.CrossRefGoogle ScholarPubMed
11.Layton, WM Jr. Random determination of a developmental process. Reversal of normal visceral asymmetry in the mouse. J Hered 1976; 67: 336–338.CrossRefGoogle ScholarPubMed
12.Layton, WM Jr. Heart malformations in mice homozygous for a gene causing situs inversus. Birth Defects 1978; 14: 277–293.Google ScholarPubMed
13.Icardo, JM, D'Vega, MJS. Spectrum of heart malformations in mice with situs solitus, situs inversus, and associated visceral heterotaxy. Circulation 1991; 84: 2547–2558.CrossRefGoogle ScholarPubMed
14.Casey, B, Devoto, M, Jones, KL, Ballabio, A. Mapping a gene for familial situs abnormalities to human chromosome Xq24–q27.1. Nature Genetics 1993; 5: 403–407.CrossRefGoogle ScholarPubMed
15.Koto, M, Adachi, J, Shimizu, A. A new mutation of primary ciliary dyskinesia with visceral inversion (Kartagener's syndrome) and hydrocephalus. In: Cramer, DV (ed). Rat News Letter No. 18, Univ. of Pittsburgh School of Med, Pittsburgh, 1987, pp 14–15.Google Scholar
16.Miura, S, Miyagawa, S, Morishima, M, Ando, M, Takao, A. Retinoic acid-induced visceral heterotaxy syndrome in rat embryos. In: Clark, EB, Takao, A (eds). Developmental Cardiology: Morphogenesis and function. Futura Publishing, Mount Kisco, NY, 1990, pp 467–484.Google Scholar
17.Horwich, A, Brueckner, M. Left, right and without a cue. Nature Genetics 1993; 5: 321–322.CrossRefGoogle ScholarPubMed
18.Haris, C, Juchau, MR, Mirkes, PE. Role of glutathion and Hsp 70 in the acquisition of thermotolerance in postimplantation rat embryos. Teratology 1991; 43: 229–239.CrossRefGoogle Scholar
19.Mirkes, PE, Doggett, B. Accumulation of heat shock protein 72 (hsp 72) in postimplantation rat embryos after exposure to various periods of hyperthermia (40–43 °C) in vitro: evidence that heat shock protein 72 is a biomarker of heat-induced embryotoxicity. Teratology 1992; 46: 301–309.CrossRefGoogle Scholar
20.Heikkila, JJ. Heat shock gene expression and development. II. An overview of mammalian and avian developmental systems. Dev Gene 1993; 14: 87–91.CrossRefGoogle Scholar
21.Walsh, D, Li, K, Wass, J, Dolnikov, A, Zeng, F, Zhe, L, Edwards, M. Heat-shock gene expression and cell cycle changes during mammalian embryonic development. Dev Gene 1993; 14: 127–136.CrossRefGoogle ScholarPubMed