NO prevents neutrophil-mediated pulmonary vasomotor dysfunction in acute lung injury

Randall S. Friese; David A. Fullerton; Robert C. Mcintyre; Thomas F. Rehring; Jeanette Agrafojo; Anirban Banerjee; Alden H. Harken

doi:10.1006/jsre.1996.0216

NO prevents neutrophil-mediated pulmonary vasomotor dysfunction in acute lung injury

Randall S. Friese, David A. Fullerton, Robert C. Mcintyre, Thomas F. Rehring, Jeanette Agrafojo, Anirban Banerjee, Alden H. Harken

Surgery

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

The purpose of this study was to examine the effect of administration of inhaled nitric oxide (NO) on lung neutrophil accumulation and pulmonary vascular endothelial cell function in endotoxin-induced acute lung injury. Mechanically ventilated rats were studied 4 hr after endotoxin (0.5 mg/kg IP). Inhaled NO (20 ppm) was administered for either the entire 4 hr after endotoxin (continuous group) or for only the first 2 of 4 hr after endotoxin (abbreviated group). Endothelial-dependent (acetylcholine, ACh) and - independent cGMP-mediated relaxation (nitroprusside, SNP) pulmonary vasorelaxation were studied in isolated pulmonary arterial rings. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). Inhaled NO prevented endotoxin-induced lung neutrophil accumulation as well as pulmonary endothelial cell dysfunction. However, this protection required continuous administration of inhaled NO. We conclude that inhaled NO prevents neutrophil-mediated pulmonary vascular endothelial cell dysfunction in acute lung injury.

Original language	English (US)
Pages (from-to)	23-28
Number of pages	6
Journal	Journal of Surgical Research
Volume	63
Issue number	1
DOIs	https://doi.org/10.1006/jsre.1996.0216
State	Published - Jun 1996

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Surgery

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10.1006/jsre.1996.0216

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title = "NO prevents neutrophil-mediated pulmonary vasomotor dysfunction in acute lung injury",

abstract = "The purpose of this study was to examine the effect of administration of inhaled nitric oxide (NO) on lung neutrophil accumulation and pulmonary vascular endothelial cell function in endotoxin-induced acute lung injury. Mechanically ventilated rats were studied 4 hr after endotoxin (0.5 mg/kg IP). Inhaled NO (20 ppm) was administered for either the entire 4 hr after endotoxin (continuous group) or for only the first 2 of 4 hr after endotoxin (abbreviated group). Endothelial-dependent (acetylcholine, ACh) and - independent cGMP-mediated relaxation (nitroprusside, SNP) pulmonary vasorelaxation were studied in isolated pulmonary arterial rings. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). Inhaled NO prevented endotoxin-induced lung neutrophil accumulation as well as pulmonary endothelial cell dysfunction. However, this protection required continuous administration of inhaled NO. We conclude that inhaled NO prevents neutrophil-mediated pulmonary vascular endothelial cell dysfunction in acute lung injury.",

author = "Friese, {Randall S.} and Fullerton, {David A.} and Mcintyre, {Robert C.} and Rehring, {Thomas F.} and Jeanette Agrafojo and Anirban Banerjee and Harken, {Alden H.}",

note = "Funding Information: 1Supported by NIH Grant R29HL49398.",

year = "1996",

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doi = "10.1006/jsre.1996.0216",

language = "English (US)",

volume = "63",

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T1 - NO prevents neutrophil-mediated pulmonary vasomotor dysfunction in acute lung injury

AU - Friese, Randall S.

AU - Fullerton, David A.

AU - Mcintyre, Robert C.

AU - Rehring, Thomas F.

AU - Agrafojo, Jeanette

AU - Banerjee, Anirban

AU - Harken, Alden H.

N1 - Funding Information: 1Supported by NIH Grant R29HL49398.

PY - 1996/6

Y1 - 1996/6

N2 - The purpose of this study was to examine the effect of administration of inhaled nitric oxide (NO) on lung neutrophil accumulation and pulmonary vascular endothelial cell function in endotoxin-induced acute lung injury. Mechanically ventilated rats were studied 4 hr after endotoxin (0.5 mg/kg IP). Inhaled NO (20 ppm) was administered for either the entire 4 hr after endotoxin (continuous group) or for only the first 2 of 4 hr after endotoxin (abbreviated group). Endothelial-dependent (acetylcholine, ACh) and - independent cGMP-mediated relaxation (nitroprusside, SNP) pulmonary vasorelaxation were studied in isolated pulmonary arterial rings. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). Inhaled NO prevented endotoxin-induced lung neutrophil accumulation as well as pulmonary endothelial cell dysfunction. However, this protection required continuous administration of inhaled NO. We conclude that inhaled NO prevents neutrophil-mediated pulmonary vascular endothelial cell dysfunction in acute lung injury.

AB - The purpose of this study was to examine the effect of administration of inhaled nitric oxide (NO) on lung neutrophil accumulation and pulmonary vascular endothelial cell function in endotoxin-induced acute lung injury. Mechanically ventilated rats were studied 4 hr after endotoxin (0.5 mg/kg IP). Inhaled NO (20 ppm) was administered for either the entire 4 hr after endotoxin (continuous group) or for only the first 2 of 4 hr after endotoxin (abbreviated group). Endothelial-dependent (acetylcholine, ACh) and - independent cGMP-mediated relaxation (nitroprusside, SNP) pulmonary vasorelaxation were studied in isolated pulmonary arterial rings. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). Inhaled NO prevented endotoxin-induced lung neutrophil accumulation as well as pulmonary endothelial cell dysfunction. However, this protection required continuous administration of inhaled NO. We conclude that inhaled NO prevents neutrophil-mediated pulmonary vascular endothelial cell dysfunction in acute lung injury.

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JO - Journal of Surgical Research

JF - Journal of Surgical Research

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NO prevents neutrophil-mediated pulmonary vasomotor dysfunction in acute lung injury

Abstract

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