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Endogenous nitric oxide and the pulmonary microvasculature in healthy sheep and during systemic inflammation.
Am J Respir Crit Care Med. 1998 May; 157(5 Pt 1):1542-9.AJ

Abstract

Nitric oxide (NO) influences microvascular integrity. NO synthase inhibitors are regarded as therapeutic options, but their impact on the pulmonary microvasculature is not well defined. We studied the microvascular effects of the nonselective NO synthase inhibitor N(omega)-nitro L-arginine methylester (L-NAME) in healthy sheep and during systemic inflammation. Permeability analysis was performed in 30 adult ewes with chronic lung lymph fistulas and pulmonary venous occluders. Experiment 1: 20 sheep received Escherichia coli endotoxin (lipopolysaccharide, 10 ng/kg/min) for 32 h. After 24 h of endotoxemia, 10 sheep were given L-NAME (25 mg/kg), and 10 sheep received NaCl 0.9%. Experiment 2: six sheep were treated with L-NAME (25 mg/kg), and four animals received NaCl 0.9%. Endotoxin induced a phasic pulmonary microvascular response with early transiently increased endothelial permeability at 4 h and late normalization of microvascular integrity to large molecules after 24 h. At that time systemic vasodilation had occurred. L-NAME raised pulmonary artery pressure and pulmonary vascular resistance index without signs of increased permeability in either experiment. NO is involved in vascular tone in healthy sheep and during systemic inflammation, but it does not seem to play a role in the integrity of the pulmonary microvascular barrier function to large molecules.

Authors+Show Affiliations

Department of Anesthesiology, The University of Texas Medical Branch, Galveston 77555-1091, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9603136

Citation

Hinder, F, et al. "Endogenous Nitric Oxide and the Pulmonary Microvasculature in Healthy Sheep and During Systemic Inflammation." American Journal of Respiratory and Critical Care Medicine, vol. 157, no. 5 Pt 1, 1998, pp. 1542-9.
Hinder F, Meyer J, Booke M, et al. Endogenous nitric oxide and the pulmonary microvasculature in healthy sheep and during systemic inflammation. Am J Respir Crit Care Med. 1998;157(5 Pt 1):1542-9.
Hinder, F., Meyer, J., Booke, M., Ehardt, J. S., Salsbury, J. R., Traber, L. D., & Traber, D. L. (1998). Endogenous nitric oxide and the pulmonary microvasculature in healthy sheep and during systemic inflammation. American Journal of Respiratory and Critical Care Medicine, 157(5 Pt 1), 1542-9.
Hinder F, et al. Endogenous Nitric Oxide and the Pulmonary Microvasculature in Healthy Sheep and During Systemic Inflammation. Am J Respir Crit Care Med. 1998;157(5 Pt 1):1542-9. PubMed PMID: 9603136.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endogenous nitric oxide and the pulmonary microvasculature in healthy sheep and during systemic inflammation. AU - Hinder,F, AU - Meyer,J, AU - Booke,M, AU - Ehardt,J S, AU - Salsbury,J R, AU - Traber,L D, AU - Traber,D L, PY - 1998/5/29/pubmed PY - 1998/5/29/medline PY - 1998/5/29/entrez SP - 1542 EP - 9 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 157 IS - 5 Pt 1 N2 - Nitric oxide (NO) influences microvascular integrity. NO synthase inhibitors are regarded as therapeutic options, but their impact on the pulmonary microvasculature is not well defined. We studied the microvascular effects of the nonselective NO synthase inhibitor N(omega)-nitro L-arginine methylester (L-NAME) in healthy sheep and during systemic inflammation. Permeability analysis was performed in 30 adult ewes with chronic lung lymph fistulas and pulmonary venous occluders. Experiment 1: 20 sheep received Escherichia coli endotoxin (lipopolysaccharide, 10 ng/kg/min) for 32 h. After 24 h of endotoxemia, 10 sheep were given L-NAME (25 mg/kg), and 10 sheep received NaCl 0.9%. Experiment 2: six sheep were treated with L-NAME (25 mg/kg), and four animals received NaCl 0.9%. Endotoxin induced a phasic pulmonary microvascular response with early transiently increased endothelial permeability at 4 h and late normalization of microvascular integrity to large molecules after 24 h. At that time systemic vasodilation had occurred. L-NAME raised pulmonary artery pressure and pulmonary vascular resistance index without signs of increased permeability in either experiment. NO is involved in vascular tone in healthy sheep and during systemic inflammation, but it does not seem to play a role in the integrity of the pulmonary microvascular barrier function to large molecules. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/9603136/Endogenous_nitric_oxide_and_the_pulmonary_microvasculature_in_healthy_sheep_and_during_systemic_inflammation_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm.157.5.9707161?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -