Necrotizing enterocolitis in a neonatal piglet model

Cohen, Ian T.; Nelson, Scarlett D.; Moxley, Rodney A.; Hirsh, Michael; Counihan, Timothy C.; Martin, Ronald F.

doi:10.1016/0022-3468(91)90716-7

Cited by 35 publications

(22 citation statements)

References 9 publications

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“…Necrotizing enterocolitis can be induced by experimental HT in newborn pigs (23); however, no gut pathology was seen in the present study. This could be explained by careful introduction of oral feed as we have previously found necrotizing enterocolitis and distended abdomen with another feeding regimes (14,24).…”

Section: Discussioncontrasting

confidence: 82%

Delayed Hypothermia as Selective Head Cooling or Whole Body Cooling Does Not Protect Brain or Body in Newborn Pig Subjected to Hypoxia-Ischemia

et al. 2008

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ABSTRACT:The neuroprotective efficacy of hypothermia (HT) after hypoxia-ischemia (HI) falls dramatically the longer the delay in initiating HT. Knowledge is scarce regarding protective or adverse effects of HT in organs beyond the brain. In addition, the relative effectiveness of selective head cooling (SHC) and whole body cooling (WBC) has not been studied. We aimed to examine whether 24 h HT, initiated 3 h after global HI is brain-and/or organ-protective using pathology, neurology, and biochemical markers. Fifty, Յ1-dold pigs were subjected to global HI causing permanent brain injury. Animals were randomized to normothermia (NT), (T rectal ) 39.0°C, SHC Trectal 34.5°C, or WBC Trectal 34.5°C for 24 h, all followed by 48 h NT. There was no difference in injury to the brain or organs between groups. There was no gender difference in brain injury but females had significantly more organs injured [2.3 (Ϯ 1.3) [mean Ϯ SD] vs. 1.4 Ϯ (1.0)]. The postinsult decline in lactate was temperature independent. However, HT animals normalized their plasma-calcium, magnesium, and potassium significantly faster than NT. Delayed SHC or WBC, initiated 3 h after HI, does not reduce pathology in the brain nor in organs. Delayed HT improves postinsult recovery of plasma-calcium, magnesium, and potassium. There were no differences in adverse effects across groups. H ypothermia (HT) after hypoxia-ischemia (HI) is neuroprotective in experimental models across different species (1-3) with both short and long-term survival (4,5) and after a delay between insult and treatment (6,7). Recent, multicenter, randomized controlled clinical trials used two cooling methods; selective head cooling (SHC) combined with mild systemic HT to rectal temperature (T rectal ) 34.5°C (Gluckman, 2005) (8) or whole body cooling (WBC) to T rectal 33.5°C (9,10). In newborn term infants with hypoxic-ischemic encephalopathy (HIE), both the methods of cooling improved neurodevelopmental outcome (11). The two larger multicenter trials of HT applied to neonates (8,9) did not aim to examine organ protection after HT; however, some cardiovascular and biochemical results were reported and no differences between cooled and noncooled infants were seen. In a smaller WBC trial by Eicher et al. (10) where less mature infants (Ն35 wk gestational age) were also included and the most profound cooling (33.0°C) of the three trials was applied, the cooled infants needed longer inotropic support than the normothermic infants. Clotting times in the cooled infants were also abnormal more often.Although most piglet models produce an insult largely confined to the brain (12), our piglets are subjected to global HI allowing examination of systemic effects of treatment interventions as well as effects on the brain. Previously, we have shown that this model displays the same type of brain and organ injury and cardiovascular responses seen in the asphyxiated infant (2,13-15). It has been suggested that SHC is superior to WBC, offering greater cortical protection and fewer adverse systemic...

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Section: Discussioncontrasting

confidence: 82%

Delayed Hypothermia as Selective Head Cooling or Whole Body Cooling Does Not Protect Brain or Body in Newborn Pig Subjected to Hypoxia-Ischemia

et al. 2008

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“…Cohen et al described a model in which newborn piglets were subjected to a hypoxic insult [50% reduction in baseline partial pressure in arterial oxygen (PaO 2 ) for 30 minutes] and hypothermic stress (core temperature reduced to 35°C for 30 minutes). After 3-4 days, approximately half of the animals developed histological changes that resembled NEC (Cohen et al, 1991). Crissinger et al developed an NEC model in 1-dayold piglets using a combination of cow formula and ischemia/reperfusion, and showed an important role for lipids in its pathogenesis (Crissinger et al, 1994).…”

Section: Development Of Nec Mouse Modelsmentioning

confidence: 99%

The development of animal models for the study of necrotizing enterocolitis

Sodhi

Richardson

Gribar

et al. 2008

Disease Models &Amp; Mechanisms

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Necrotizing enterocolitis (NEC) is the leading cause of death and long-term disability from gastrointestinal disease in preterm infants, and is characterized by acute and chronic intestinal inflammation that may lead to systemic sepsis and multi-system organ failure. NEC typically develops in the preterm infant after the administration of tube feeds, although it may occasionally be seen in full-term babies. Despite extensive clinical experience in the management of patients with NEC, the underlying cellular and molecular mechanisms leading to its development remain incompletely understood. Several animal models have therefore been developed in a variety of species in order to study the pathogenesis of NEC and to develop more effective treatment strategies. This review seeks to examine the pros and cons of animal models that have been developed in the study of NEC over the past 30 years. It will highlight the various strengths and weaknesses of experimental approaches that have been used, and discuss potential directions for the development of such models for the future.

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“…Vários modelos animais foram propostos para demonstrar a importância da hipóxia no desenvolvimento das lesões na ECN [3][4][5][6][7][8][9][10][11][12] . Barlow e Santulli 3,5 provocaram lesão intestinal em ratos recém-nascidos alimentados com leite artificial, colocando os animais em saco plástico durante 3 a 5 minutos por dia.…”

Section: Discussionunclassified

“…Hansbrough e col. 6 , utilizando cães recém-nascidos, provocaram necrose isquêmica intestinal ao produzir hipóxia com O 2 .a 10% por 2 horas. Cohen e col. 7 submeteram porcos recém-nascidos a uma pressão parcial de O 2 de 50%, conseguindo obter evidências microscópicas e macroscópicas de ECN. Caplan e col. 8 descreveram um modelo de ECN alimentando os animais com fórmula artificial e submetendo-os a 60 segundos de asfixia com 100% de nitrogênio duas vezes ao dia seguido por exposição ao frio.…”

Section: Discussionunclassified

“…A combinação de isquemia gastrointestinal, fruto de uma redistribuição do fluxo sangüíneo esplâncnico para órgãos vitais como coração e cérebro, alimentação enteral, possivelmente predispondo à lesão da camada mucosa e mais a translocação de bactérias patogênicas, tudo isto associado a uma imaturidade dos mecanismos imunitários intestinais, estariam envolvidos em seu desenvolvimento 1,2 . Muitos modelos animais foram usados para avaliar os efeitos da hipóxia na etiopatogenia da ECN e demonstraram que o decréscimo da perfusão intestinal e que a lesão tecidual seriam causadas por um mecanismo de isquemia e reperfusão [3][4][5][6][7][8][9][10][11][12] . O objetivo de nosso estudo é avaliar um modelo experimental de ECN em ratos proposto por em 1995 por Okur e col. 9 .…”

Section: Introductionunclassified

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Avaliação de um modelo experimental de enterocolite necrosante neonatal em ratos

et al. 2006

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OBJETIVO: Avaliar um modelo experimental de enterocolite necrosante em ratos proposto por Okur e colaboradores em 1995. MÉTODOS: Utilizou-se 28 ratos da raça EPM-Wistar no primeiro dia de vida, com peso entre 4 a 6 gramas. Os animais foram submetidos a hipóxia (H) colocando os filhotes em uma câmara de gás CO2 para sacrifício de roedores onde receberam um fluxo de ar contendo 100% de CO2 durante 5 minutos. Após a hipóxia os animais foram reanimados (R) com fluxo de ar contendo O2 a 100%, também durante 5 minutos. Os animais divididos em dois grupos: G1: controle (n=12): ratos não submetidos a H-R; G2: (n=16): ratos submetidos a H-R. Segmentos de intestino delgado e cólon foram preparados para análise histológica. O restante do intestino foi utilizado para dosagem de malondialdeído tecidual. RESULTADOS: Dosagem de malondialdeído do G1 foi em média 1,05 (0,44-2,03) e do G2 foi em média 2,60 (0,59- 6,4) nmol MDA/mg proteína. O G2 teve média significativamente maior do que a do grupo controle (p<0,002). Foi encontrada diferença estatisticamente significante entre os grupos de estudo quanto à distribuição do grau de lesão onde o grupo G1 apresentou graus significantemente menores do que o grupo G2. CONCLUSÕES: O modelo mostrou que a hipóxia neonatal em ratos provoca lesões na parede intestinal.. Apesar das lesões histológicas discretas é um bom método para avaliação da liberação de radicais livres teciduais.

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Necrotizing enterocolitis in a neonatal piglet model

Cited by 35 publications

References 9 publications

Delayed Hypothermia as Selective Head Cooling or Whole Body Cooling Does Not Protect Brain or Body in Newborn Pig Subjected to Hypoxia-Ischemia

Delayed Hypothermia as Selective Head Cooling or Whole Body Cooling Does Not Protect Brain or Body in Newborn Pig Subjected to Hypoxia-Ischemia

The development of animal models for the study of necrotizing enterocolitis

Avaliação de um modelo experimental de enterocolite necrosante neonatal em ratos

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