Ventilatory response to hypoxia during endotoxemia in young rats: Role of nitric oxide

John Ladino, Eduardo Bancalari, Cleide Suguihara

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (VE) and oxygen consumption (Vo2) were measured in room air (RA) and during 30 min of hypoxia (10% O2) before and after E. coli endotoxin administration. During endotoxemia, animals received placebo (PL, n = 8); a nonselective nitric oxide synthase (NOS) inhibitor (N-nitro-L-arginine methyl ester, L-NAME, n = 9), or a neuronal NOS (nNOS) inhibitor (7-nitroindazole, 7-NI, n = 9). During endotoxemia, a larger increase in VE was observed only during the first min of hypoxia in the L-NAME group when compared with PL or 7-NI (p < 0.001). VRH was similar in the PL and 7-NI groups. A larger decrease in Vo2 at 30 min of hypoxia was observed in L-NAME and 7-NI groups when compared with PL (p < 0.03). These data demonstrate that the attenuation of the early VRH during endotoxemia is in part mediated by an inhibitory effect of endothelial NO on the respiratory control mechanisms.

Original languageEnglish (US)
Pages (from-to)134-138
Number of pages5
JournalPediatric Research
Volume62
Issue number2
DOIs
StatePublished - Aug 1 2007
Externally publishedYes

Fingerprint

Endotoxemia
Nitric Oxide
NG-Nitroarginine Methyl Ester
Ventilation
Carotid Body
Hypoxia
Oxygen Consumption
Nitric Oxide Synthase
Sepsis
Air
Placebos

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health

Cite this

Ladino, John ; Bancalari, Eduardo ; Suguihara, Cleide. / Ventilatory response to hypoxia during endotoxemia in young rats : Role of nitric oxide. In: Pediatric Research. 2007 ; Vol. 62, No. 2. pp. 134-138.
@article{38b66e16f6d2420eaee915c95dc67817,
title = "Ventilatory response to hypoxia during endotoxemia in young rats: Role of nitric oxide",
abstract = "Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (VE) and oxygen consumption (Vo2) were measured in room air (RA) and during 30 min of hypoxia (10{\%} O2) before and after E. coli endotoxin administration. During endotoxemia, animals received placebo (PL, n = 8); a nonselective nitric oxide synthase (NOS) inhibitor (N-nitro-L-arginine methyl ester, L-NAME, n = 9), or a neuronal NOS (nNOS) inhibitor (7-nitroindazole, 7-NI, n = 9). During endotoxemia, a larger increase in VE was observed only during the first min of hypoxia in the L-NAME group when compared with PL or 7-NI (p < 0.001). VRH was similar in the PL and 7-NI groups. A larger decrease in Vo2 at 30 min of hypoxia was observed in L-NAME and 7-NI groups when compared with PL (p < 0.03). These data demonstrate that the attenuation of the early VRH during endotoxemia is in part mediated by an inhibitory effect of endothelial NO on the respiratory control mechanisms.",
author = "John Ladino and Eduardo Bancalari and Cleide Suguihara",
year = "2007",
month = "8",
day = "1",
doi = "10.1203/PDR.0b013e318098721a",
language = "English (US)",
volume = "62",
pages = "134--138",
journal = "Pediatric Research",
issn = "0031-3998",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

Ventilatory response to hypoxia during endotoxemia in young rats : Role of nitric oxide. / Ladino, John; Bancalari, Eduardo; Suguihara, Cleide.

In: Pediatric Research, Vol. 62, No. 2, 01.08.2007, p. 134-138.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Ventilatory response to hypoxia during endotoxemia in young rats

T2 - Role of nitric oxide

AU - Ladino, John

AU - Bancalari, Eduardo

AU - Suguihara, Cleide

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (VE) and oxygen consumption (Vo2) were measured in room air (RA) and during 30 min of hypoxia (10% O2) before and after E. coli endotoxin administration. During endotoxemia, animals received placebo (PL, n = 8); a nonselective nitric oxide synthase (NOS) inhibitor (N-nitro-L-arginine methyl ester, L-NAME, n = 9), or a neuronal NOS (nNOS) inhibitor (7-nitroindazole, 7-NI, n = 9). During endotoxemia, a larger increase in VE was observed only during the first min of hypoxia in the L-NAME group when compared with PL or 7-NI (p < 0.001). VRH was similar in the PL and 7-NI groups. A larger decrease in Vo2 at 30 min of hypoxia was observed in L-NAME and 7-NI groups when compared with PL (p < 0.03). These data demonstrate that the attenuation of the early VRH during endotoxemia is in part mediated by an inhibitory effect of endothelial NO on the respiratory control mechanisms.

AB - Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (VE) and oxygen consumption (Vo2) were measured in room air (RA) and during 30 min of hypoxia (10% O2) before and after E. coli endotoxin administration. During endotoxemia, animals received placebo (PL, n = 8); a nonselective nitric oxide synthase (NOS) inhibitor (N-nitro-L-arginine methyl ester, L-NAME, n = 9), or a neuronal NOS (nNOS) inhibitor (7-nitroindazole, 7-NI, n = 9). During endotoxemia, a larger increase in VE was observed only during the first min of hypoxia in the L-NAME group when compared with PL or 7-NI (p < 0.001). VRH was similar in the PL and 7-NI groups. A larger decrease in Vo2 at 30 min of hypoxia was observed in L-NAME and 7-NI groups when compared with PL (p < 0.03). These data demonstrate that the attenuation of the early VRH during endotoxemia is in part mediated by an inhibitory effect of endothelial NO on the respiratory control mechanisms.

UR - http://www.scopus.com/inward/record.url?scp=34547640474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34547640474&partnerID=8YFLogxK

U2 - 10.1203/PDR.0b013e318098721a

DO - 10.1203/PDR.0b013e318098721a

M3 - Article

C2 - 17597656

AN - SCOPUS:34547640474

VL - 62

SP - 134

EP - 138

JO - Pediatric Research

JF - Pediatric Research

SN - 0031-3998

IS - 2

ER -