Alterations in Brain Structure After Asphyxiation at Birth

Windle, William F.; Becker, Robert J.; Weil, Arthur

doi:10.1097/00005072-194407000-00003

Cited by 92 publications

(16 citation statements)

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“…Windle and colleagues produced intrauterine total asphyxia in fullterm guinea pig fetuses by occluding either the umbilical cord or the maternal uterine artery [1,27,28]. Another technique was employed by Miller in his studies of survival time during neonatal asphyxia [16][17][18].…”

Section: Discussionmentioning

confidence: 99%

Brain Prostaglandins E2 and F2α following Neonatal Asphyxia in the Guinea Pig

Allen¹,

Louis²,

Kopelman

1982

Neonatology

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In this study, the effects of (1) asphyxia and (2) asphyxiation followed by resuscitation on brain levels of prostaglandins E₂ and F_2α were evaluated in 2-day-old guinea pigs. Asphyxiation in a nitrogen atmosphere for either 3 min or 3 min 40 s did not alter brain PGF_2α levels but after 3 min 40 s of asphyxia, brain PGE₂ levels were significantly elevated from control values. When asphyxiation was followed by resuscitation with 95% 0₂ and 5% CO₂, brain PGF_2α levels rose significantly while PGE₂ levels were not different from nonasphyxiated control values. Pretreatment of animals with indomethacin lowered brain levels of both prostaglandins below nonasphyxiated control levels and prevented any asphyxiation or resuscitation-induced rise in brain prostaglandin levels. Also, animals which were asphyxiated, resuscitated, and sacrificed 1 day after asphyxiation had brain prostaglandin levels which were not different from levels in nonasphyxiated control animals. These studies demonstrate a significant rise in brain PGF_2α levels following resuscitation from acute total asphyxia. We speculate that the resuscitation-induced rise in brain PGF_2α may contribute to restriction of cerebral blood flow in the postasphyxial period through its action as a vasoconstrictive agent.

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Section: Discussionmentioning

confidence: 99%

Brain Prostaglandins E2 and F2α following Neonatal Asphyxia in the Guinea Pig

Allen¹,

Louis²,

Kopelman

1982

Neonatology

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“…This relationship is significant only for speech recognition but not for pure-tone hearing thresholds or sound localization. This is surprising because research using animal models has shown a relationship between asphyxiation at birth and hearing loss (e.g., Meyers, 1969;Windle, Becker, & Weil, 1944). Study of humans, however, has shown that asphyxiation at birth is only likely to play a significant role in producing hearing loss if it appears in combination with other birth stressors, such as repeated episodes of acidosis (Despland & Galambos, 1982;Gunn, Cook, Williams, Johnston, & Gluckman, 1991), encephalopathy (Robertson & Finer, 1993), or other multiple risk factors (Duara, Suter, Bessard, & Gutberlet, 1986;Gupta, Anand, & Raj, 1991).…”

Section: Relative Impact Of Birth Risk Factorsmentioning

confidence: 99%

Adult Sensory Capacities as a Function of Birth Risk Factors

Harland

Coren²

1996

Journal of Clinical and Experimental Neuropsychology

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This study examined the relationship between birth risk factors and sensory capacity in 1245 young adults (mean age = 19.9 years). Nine birth risk factors were included (long labour, breech birth, breathing difficulty, instrument delivery, Caesarian delivery, multiple birth, premature birth, low birth weight, and high-risk birth order) and six sensory capacities were tested (Snellen visual acuity, stereopsis, color discrimination, pure-tone hearing, speech recognition, and sound localization). Mild birth stressors were strongly predictive of reduced visual acuity and stereoscopic discrimination, and mildly predictive for the other sensory measures. The fact that vision was more vulnerable to the effects of birth stress than audition may be due to the slower maturation of the visual system. Of the birth stressors examined, twinning was found to have the largest effect on sensory function, possibly because it often occurs conjointly with other birth stressors such as low birth weight, breech presentation, and breathing difficulty and may involve the use of birthing instruments such as forceps.

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“…Since then a large number of workers have assigned various reasons to the appearance of 'dark' cells. A few important ones are: postmortem changes (Scharer 1938), asphyxia (Windle et al 1944;Rand and CourvilIe 1946), damaging effect of the fixatives (Gerhard et al1948) and regeneration or recovery phase (Bohra and Gupta 1983). The present study reveals a relationship of the appearance of 'dark' cells with the ageing of animals in the cerebellar cortex of Wistar rats-a relationship established never before.…”

Section: Introductionmentioning

confidence: 99%

‘Dark’ type Purkinje cells and neuronal ageing

Sharma

Patro

James

1988

Proc. Indian Acad. Sci. (Anim. Sci.)

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Eighty Wistar rats from age-groups of 3, 12 and 36 months were selected at random from the inbred colony. Ten animals from each group were treated with the ageingreversal drug, centrophenoxine (lOO mg/kg/day, intraperitoneally for 10 weeks). The Purkinje cell population of the brain of these animals were scanned histopathologically to record the impact of chronological age on the rate of conversion of 'light' into 'dark' type. The population of 'dark' cells increased by 52% from 3-36 months. The 'dark' neurons, even in the 3 month-old animals had substantial amount of histochemically detectable and autofluorescent age-pigment. While centrophenoxine could remove most of the pigment present in the 'light' type Purkinje neurons it failed to influence the pigment in any way in the 'dark' cells. The drug could not also influence the conversion of the 'light' cells into 'dark' type.

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Alterations in Brain Structure After Asphyxiation at Birth

Cited by 92 publications

References 0 publications

Brain Prostaglandins E<sub>2</sub> and F<sub>2α</sub> following Neonatal Asphyxia in the Guinea Pig

Brain Prostaglandins E<sub>2</sub> and F<sub>2α</sub> following Neonatal Asphyxia in the Guinea Pig

Adult Sensory Capacities as a Function of Birth Risk Factors

‘Dark’ type Purkinje cells and neuronal ageing

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