Regulations during survival without oxygen in infant mammals

Adolph, E. F.

doi:10.1016/0034-5687(69)90019-x

Cited by 64 publications

(53 citation statements)

References 18 publications

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“…Yet, as noted above, some groups of investigators have argued that the rhythmic activity of this preparation is similar to the eupnoeic pattern of the in vivo neonatal rat (Smith et al 1990Greer, Smith & Feldman, 1991;Brockhaus et al 1993). However, the rhythmic neural discharges of the in vitro preparation appear to correspond more closely to gasping, as described in adult (Adolf & Hoy, 1960;Stafford & Weatherall, 1960;Adolf, 1969). The pattern of rhythmic activity of the in vitro preparation is unalterable, except to apnoea (Suzue, 1984;Murakoshi et al 1985;Smith et al 1990Smith et al , 1991Brockhaus et al 1993;Okada, Muckenhoff & Scheid, 1993b).…”

Section: Discussionmentioning

confidence: 62%

Medullary loci critical for expression of gasping in adult rats.

Fung

Wang

John

1994

The Journal of Physiology

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1. Our purpose was to define whether a region of medulla could be identified that is critical for the expression of gasping. 2. Decerebrate, vagotomized, paralysed and ventilated adult rats were used. The pattern of phrenic activity was reversibly altered from eupnoea to gasping by exposure to hypoxia or anoxia. 3. Gasping was irreversibly eliminated following unilateral electrolytic lesions of the lateral tegmental field of the medulla. The eupnoeic rhythm continued after these lesions. 4. Injections of kainic acid into the lateral tegmental field also eliminated gasping. Phrenic activity in eupnoea was not altered. 5. Lesions outside the lateral tegmental field caused marked changes in the eupnoeic rhythm, including expiratory apnoea. Upon exposure to hypoxia or anoxia, gasping was still induced. 6. This region for the neurogenesis of gasping in rats is identical to the region that serves a comparable function in cats. Moreover, it overlaps with the ‘pre‐Bötzinger’ complex which has been described for the in vitro brainstem preparation of the neonatal rat. Our results raise doubts that this complex plays a role in the neurogenesis of eupnoea.

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Section: Discussionmentioning

confidence: 62%

Medullary loci critical for expression of gasping in adult rats.

Fung

Wang

John

1994

The Journal of Physiology

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“…Young animals should exhibit better adaptability to hypoxia than adults due to their initial higher CNS levels of taurine. In addition, the long time required for adaptation to hypoxia in vitro [24] and the slow decline (days) in the resistance to hypoxia in newborn rats [57] could be due to the slow turnover of taurine. Our hypothesis predicts that animals with inherently low levels of taurine or those in which taurine biosynthesis is defective, will be highly sensitive to hypoxia.…”

Section: Discussionmentioning

confidence: 99%

The mechanism of neuronal resistance and adaptation to hypoxia

Schurr

Rigor

1987

FEBS Letters

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In this work we provide a theoretical explanation for the observations that: (i) young animals are more resistant to hypoxia than adult ones and (ii) repeated exposure to a hypoxic insult increases the tolerance of young animals and isolated brain tissue to that insult. Considered here is the role of taurine, a putative Ca 2+ transport modulator, in attenuating Ca 2+ influx and overload in brain tissue upon hypoxia. It is proposed that the higher resistance of young animals to hypoxia stems from their higher brain content of taurine as compared with adults. The increased resistance to lack of oxygen upon re-exposure to hypoxia may occur as a result of protein and coenzyme A (CoA) breakdown which leads to the accumulation of products like cystine, cysteine, cysteamine and other sulfur-containing compounds. Upon reoxygenation, these compounds are oxidized to form taurine, which in turn attenuates neuronal Ca 2+ accumulation. The sulfurcontaining compounds are considered to be natural scavengers of oxygen-derived free radicals which are formed upon reoxygenation and have been implicated as a major component in the process leading to ischemic/hypoxic brain damage. Repeated hypoxic insults bring about the formation of higher levels of taurine and hence the observed adaptation to oxygen lack. The hypothesis presented here is supported by experimental observations in our laboratory and those of others.

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“…the ability to use lactate as a substrate for glycolysis (30) and to divert energy resources away from nonessential processes of growth (31,32). These mechanisms are gradually lost as the animal matures (33).…”

Section: Litter Size and Neonatal Brain Injurymentioning

confidence: 99%

The Influence of Litter Size on Brain Damage Caused by Hypoxic-Ischemic Injury in the Neonatal Rat

OAKDEN

2002

Pediatric Research

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Hypoxic ischemia is a common cause of brain injury in the human neonate. This can be mimicked in the neonatal rat, but produces variable injury. The present study investigated the influence of litter size on the severity and variability of damage caused by hypoxic-ischemic injury in neonatal rats. Groups of 7-d-old pups from birth-sized litters (13-15 pups), or from litters culled to 10 on postnatal d 2, and 8-and 9-d-old pups from birth-sized litters, were exposed to common carotid artery occlusion and then, 3 h later, hypoxia (2 h 15 min, 8% oxygen). Damage was assessed histologically 72 h after injury, and graded (I-IV) according to severity. In nonculled litters, similar numbers of animals had each grade of injury. Most pups (70%) from culled litters had grade III or IV damage, and severity was significantly greater than in nonculled litters (p Ͻ 0.001). Pups from culled litters were heavier (17.6 Ϯ 0.4 g) than pups from nonculled litters (14.7 Ϯ 0.3 g, p Ͻ 0.0001). To determine whether this indicated that culled litters were more similar to older pups in their response to hypoxic-ischemic injury, we examined injury in 8-and 9-d-old pups of similar body weight to 7-d-old pups from culled litters. The severity and distribution of damage in the older pups was different from damage in the 7-d-old pups from culled litters. These data suggest that in 7-d-old rats, litter size influences damage caused by hypoxicischemic injury, and that the relationship between body weight, brain development, and susceptibility to hypoxic-ischemic injury is complex. Hypoxic-ischemic injury in neonates occurs as a result of intrauterine hypoxia and birth asphyxia and is a significant cause of death and disability (1, 2). To study the mechanisms underlying hypoxic-ischemic injury in the laboratory setting, the injury can be mimicked in the neonatal rat (3).A commonly used animal model to study perinatal hypoxicischemic brain damage is the 7-d-old rat subjected to unilateral common carotid ligation followed by exposure to 8% oxygen (4, 5).The severity of damage caused by hypoxic-ischemic injury in the 7-d-old rat is variable, often requiring 25-30 animals per group, and a similar number of controls, to test treatments and interventions (6 -9). Variation is reportedly limited by using pups of similar body weight (10 -12), and several studies have culled litters, possibly to reduce variation in body weight (10, 13, 14), but no universal protocol has been followed. A previous study observed that pups assigned to litters of six on postnatal d 1 (P1), were more susceptible to injury on P7 than those from litters of 14 (6). However, in this study, damage was assessed by measurement of brain size.Thus, the aim of the present study was to investigate in more detail the effect of culling litters on the damage caused by hypoxic-ischemic injury in the 7-d-old rat, and to determine the relationship between body weight and injury severity in culled and nonculled litters. Pups from culled litters were found to be heavier than those from birth-size...

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Regulations during survival without oxygen in infant mammals

Cited by 64 publications

References 18 publications

Medullary loci critical for expression of gasping in adult rats.

Medullary loci critical for expression of gasping in adult rats.

The mechanism of neuronal resistance and adaptation to hypoxia

The Influence of Litter Size on Brain Damage Caused by Hypoxic-Ischemic Injury in the Neonatal Rat

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