Effects of chronic hypercapnia in the neonatal mouse lung and brain

Sumon Das, Zhongfang Du, Shira Bassly, Lewis Singer, Alfin G. Vicencio

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Summary. Background: Permissive hypercapnia is increasingly utilized in the care of premature infants to prevent bronchopulmonary dysplasia. In a previous investigation, we described gene expression changes in the neonatal mouse lung exposed to chronic hypercapnia that might contribute to lung protection and accelerated maturation. However, it is unknown whether chronic hypercapnia increases alveolar formation, nor if it has detrimental effects in other developing organs such as the brain. Objective: To determine whether chronic hypercapnia accelerates early alveolar formation and increases neuronal cell injury in the developing mouse lung and brain, respectively Design: Mouse pups were exposed to 8% CO 2 + 21% O 2 starting at postnatal day (P) 2 until P7. Control animals were maintained in room air. Animals were sacrificed at P4 or P7, and lungs and brains were excised and analyzed. Results: Exposure to 8% CO 2 resulted in an increased expression of α-smooth muscle actin (α-sma) which localized to the tips of developing alveolar buds, and also an increased number of alveolar buds at P7. Importantly, hypercapnic animals also demonstrated evidence of increased TUNEL-positive cells in the brain. Conclusions: Exposure to chronic hypercapnia may lead to early initiation of alveolar budding in the neonatal mouse, but may also lead to increased TUNEL- positive cells in the developing brain.

Original languageEnglish (US)
Pages (from-to)176-182
Number of pages7
JournalPediatric Pulmonology
Volume44
Issue number2
DOIs
StatePublished - Feb 2009

Fingerprint

Hypercapnia
Lung
Brain
In Situ Nick-End Labeling
Carbon Monoxide
Bronchopulmonary Dysplasia
Premature Infants
Smooth Muscle
Actins
Air
Gene Expression
Wounds and Injuries

Keywords

  • Alveolar development
  • Cell injury
  • Permissive hypercapnia
  • TUNEL

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Pulmonary and Respiratory Medicine

Cite this

Das, S., Du, Z., Bassly, S., Singer, L., & Vicencio, A. G. (2009). Effects of chronic hypercapnia in the neonatal mouse lung and brain. Pediatric Pulmonology, 44(2), 176-182. https://doi.org/10.1002/ppul.20971

Effects of chronic hypercapnia in the neonatal mouse lung and brain. / Das, Sumon; Du, Zhongfang; Bassly, Shira; Singer, Lewis; Vicencio, Alfin G.

In: Pediatric Pulmonology, Vol. 44, No. 2, 02.2009, p. 176-182.

Research output: Contribution to journalArticle

Das, S, Du, Z, Bassly, S, Singer, L & Vicencio, AG 2009, 'Effects of chronic hypercapnia in the neonatal mouse lung and brain', Pediatric Pulmonology, vol. 44, no. 2, pp. 176-182. https://doi.org/10.1002/ppul.20971
Das, Sumon ; Du, Zhongfang ; Bassly, Shira ; Singer, Lewis ; Vicencio, Alfin G. / Effects of chronic hypercapnia in the neonatal mouse lung and brain. In: Pediatric Pulmonology. 2009 ; Vol. 44, No. 2. pp. 176-182.
@article{2ad42502dc2243cda5a86698d390c6cb,
title = "Effects of chronic hypercapnia in the neonatal mouse lung and brain",
abstract = "Summary. Background: Permissive hypercapnia is increasingly utilized in the care of premature infants to prevent bronchopulmonary dysplasia. In a previous investigation, we described gene expression changes in the neonatal mouse lung exposed to chronic hypercapnia that might contribute to lung protection and accelerated maturation. However, it is unknown whether chronic hypercapnia increases alveolar formation, nor if it has detrimental effects in other developing organs such as the brain. Objective: To determine whether chronic hypercapnia accelerates early alveolar formation and increases neuronal cell injury in the developing mouse lung and brain, respectively Design: Mouse pups were exposed to 8{\%} CO 2 + 21{\%} O 2 starting at postnatal day (P) 2 until P7. Control animals were maintained in room air. Animals were sacrificed at P4 or P7, and lungs and brains were excised and analyzed. Results: Exposure to 8{\%} CO 2 resulted in an increased expression of α-smooth muscle actin (α-sma) which localized to the tips of developing alveolar buds, and also an increased number of alveolar buds at P7. Importantly, hypercapnic animals also demonstrated evidence of increased TUNEL-positive cells in the brain. Conclusions: Exposure to chronic hypercapnia may lead to early initiation of alveolar budding in the neonatal mouse, but may also lead to increased TUNEL- positive cells in the developing brain.",
keywords = "Alveolar development, Cell injury, Permissive hypercapnia, TUNEL",
author = "Sumon Das and Zhongfang Du and Shira Bassly and Lewis Singer and Vicencio, {Alfin G.}",
year = "2009",
month = "2",
doi = "10.1002/ppul.20971",
language = "English (US)",
volume = "44",
pages = "176--182",
journal = "Pediatric Pulmonology",
issn = "8755-6863",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Effects of chronic hypercapnia in the neonatal mouse lung and brain

AU - Das, Sumon

AU - Du, Zhongfang

AU - Bassly, Shira

AU - Singer, Lewis

AU - Vicencio, Alfin G.

PY - 2009/2

Y1 - 2009/2

N2 - Summary. Background: Permissive hypercapnia is increasingly utilized in the care of premature infants to prevent bronchopulmonary dysplasia. In a previous investigation, we described gene expression changes in the neonatal mouse lung exposed to chronic hypercapnia that might contribute to lung protection and accelerated maturation. However, it is unknown whether chronic hypercapnia increases alveolar formation, nor if it has detrimental effects in other developing organs such as the brain. Objective: To determine whether chronic hypercapnia accelerates early alveolar formation and increases neuronal cell injury in the developing mouse lung and brain, respectively Design: Mouse pups were exposed to 8% CO 2 + 21% O 2 starting at postnatal day (P) 2 until P7. Control animals were maintained in room air. Animals were sacrificed at P4 or P7, and lungs and brains were excised and analyzed. Results: Exposure to 8% CO 2 resulted in an increased expression of α-smooth muscle actin (α-sma) which localized to the tips of developing alveolar buds, and also an increased number of alveolar buds at P7. Importantly, hypercapnic animals also demonstrated evidence of increased TUNEL-positive cells in the brain. Conclusions: Exposure to chronic hypercapnia may lead to early initiation of alveolar budding in the neonatal mouse, but may also lead to increased TUNEL- positive cells in the developing brain.

AB - Summary. Background: Permissive hypercapnia is increasingly utilized in the care of premature infants to prevent bronchopulmonary dysplasia. In a previous investigation, we described gene expression changes in the neonatal mouse lung exposed to chronic hypercapnia that might contribute to lung protection and accelerated maturation. However, it is unknown whether chronic hypercapnia increases alveolar formation, nor if it has detrimental effects in other developing organs such as the brain. Objective: To determine whether chronic hypercapnia accelerates early alveolar formation and increases neuronal cell injury in the developing mouse lung and brain, respectively Design: Mouse pups were exposed to 8% CO 2 + 21% O 2 starting at postnatal day (P) 2 until P7. Control animals were maintained in room air. Animals were sacrificed at P4 or P7, and lungs and brains were excised and analyzed. Results: Exposure to 8% CO 2 resulted in an increased expression of α-smooth muscle actin (α-sma) which localized to the tips of developing alveolar buds, and also an increased number of alveolar buds at P7. Importantly, hypercapnic animals also demonstrated evidence of increased TUNEL-positive cells in the brain. Conclusions: Exposure to chronic hypercapnia may lead to early initiation of alveolar budding in the neonatal mouse, but may also lead to increased TUNEL- positive cells in the developing brain.

KW - Alveolar development

KW - Cell injury

KW - Permissive hypercapnia

KW - TUNEL

UR - http://www.scopus.com/inward/record.url?scp=59949098576&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=59949098576&partnerID=8YFLogxK

U2 - 10.1002/ppul.20971

DO - 10.1002/ppul.20971

M3 - Article

C2 - 19142892

AN - SCOPUS:59949098576

VL - 44

SP - 176

EP - 182

JO - Pediatric Pulmonology

JF - Pediatric Pulmonology

SN - 8755-6863

IS - 2

ER -