Principles Governing the Genesis of Congenital Malformations Induced in Mice by Hypoxia

Ingalls, Theodore H.; Curley, Francis J.

doi:10.1056/nejm195712052572306

Cited by 110 publications

(26 citation statements)

References 8 publications

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“…In growing organs the manifestations differ with the stage of development [Ingalls and C urley, 1957]. The effect may be direct or indirect and be reflected in e. g. damage to the central nervous system or changes in hormonal production [M arks, B hattacharya and V ernikos-D anellis, 1965], In the cell, hypoxia acts on the respiratory apparatus resulting in depressed cellular function and finally irreversible damage [G rabow ski, 1964;Stave, 1965].…”

Section: Discussionmentioning

confidence: 99%

“…

Hypoxia or anoxia has been shown to be capable of causing intrauter ine death, congenital malformations and cerebral disorders in experimen tal animals [H urder and Sanders, 1953; Murakami, Kameyama and Kato, 1955;Ingalls and C urley, 1957]. Rabbit embryos exposed to experimental conditions simulating the oxygen deficiency at high altitudes develop severe craniofacial dysplasia and dental defects, namely enamel and dentine hypoplasia [Degenhardt, I960].

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confidence: 99%

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Influence of Experimental Brief Perinatal Hypoxia on the Rat Incisor

Magnusson¹,

Hänström²,

Grahnén³

1969

Caries Res

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Section: Discussionmentioning

confidence: 99%

“…

…”

mentioning

confidence: 99%

Influence of Experimental Brief Perinatal Hypoxia on the Rat Incisor

Magnusson¹,

Hänström²,

Grahnén³

1969

Caries Res

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“…It may not be clinically evident at birth but develops until adolescence [3]. Genes that are associated with vertebral malformation have been identified in several studies [4][5][6], and similar defects have been induced in animal models by hypoxia or toxic agents [7,8].…”

Section: Introductionmentioning

confidence: 99%

Epidemiology of adolescent idiopathic scoliosis

Konieczny

Senyurt

Krauspe

2013

Journal of Children's Orthopaedics

771

550

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Adolescent idiopathic scoliosis is a common disease with an overall prevalence of 0.47-5.2 % in the current literature. The female to male ratio ranges from 1.5:1 to 3:1 and increases substantially with increasing age. In particular, the prevalence of curves with higher Cobb angles is substantially higher in girls than in boys: The female to male ratio rises from 1.4:1 in curves from 10°to 20°up to 7.2:1 in curves [40°. Curve pattern and prevalence of scoliosis is not only influenced by gender, but also by genetic factors and age of onset. These data obtained from school screening programs have to be interpreted with caution, since methods and cohorts of the different studies are not comparable as age groups of the cohorts and diagnostic criteria differ substantially. We do need data from studies with clear standards of diagnostic criteria and study protocols that are comparable to each other.

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“…References: almokalant [28] and Sköld et al unpublished, and hypoxia [18][19][20][21][22][23][24][25][26] developmental stage of the induced oxygen deficiency advanced [22][23][24][25][26].…”

Section: Skeletal Defectsmentioning

confidence: 99%

Class III Antiarrhythmics and Phenytoin: Teratogenicity Due to Embryonic Cardiac Dysrhythmia and Reoxygenation Damage

Danielsson¹,

Sköld²,

Azarbayjani³

2001

CPD

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Class III antiarrhythmic drugs, like almokalant, dofetilide and ibutilide, cause a spectrum of malformations in experimental teratology studies. The pattern of developmental toxic effects is very similar to those reported for phenytoin, which is an established human and animal teratogen. The toxic effects are characterised by embryonic death, decreased fetal weights, and stage specific malformations, such as distal digital reductions, orofacial clefts and cardiovascular defects. Class III antiarrhythmics decrease the excitability of cardiac cells by selectively blocking the rapid component of the delayed rectified potassium channel (IKr), resulting in prolongation of the repolarisation phase of the action potential. Phenytoin, which decrease the excitability of neurones, has recently also been shown to block IKr, in addition to its known blockade of sodium channels. Animal studies indicate that IKr is expressed in the embryo and that the embryonic heart is extremely susceptible to IKr-blockers during a restricted period in early development. At concentrations not affecting the maternal heart, the embryonic heart reacts with bradycardia, arrhythmia and cardiac arrest when exposed to such drugs. Available studies strongly support the idea that birth defects after in utero exposure to both selective and non-selective IKr-blockers (like phenytoin) are initiated by concentration dependent embryonic bradycardia/arrhythmia resulting in 1) hypoxia; explaining embryonic death and growth retardation, 2) episodes of severe hypoxia, followed by generation of reactive oxygen species within the embryo during reoxygenation, causing orofacial clefts and distal digital reductions, and 3) alterations in embryonic blood flow and blood pressure, inducing cardiovascular defects.

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Principles Governing the Genesis of Congenital Malformations Induced in Mice by Hypoxia

Cited by 110 publications

References 8 publications

Influence of Experimental Brief Perinatal Hypoxia on the Rat Incisor

Influence of Experimental Brief Perinatal Hypoxia on the Rat Incisor

Epidemiology of adolescent idiopathic scoliosis

Class III Antiarrhythmics and Phenytoin: Teratogenicity Due to Embryonic Cardiac Dysrhythmia and Reoxygenation Damage

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