Advanced

Inhaled nitric oxide reveals and attenuates endothelial dysfunction after lung transplantation

Lindberg, Lars LU ; Kimblad, Per Ola LU ; Sjöberg, Trygve LU ; Ingemansson, Richard LU and Steen, Stig LU (1996) In Annals of Thoracic Surgery 62(6). p.1639-1643
Abstract
BACKGROUND: Maintaining endothelial function within transplanted organs may be critical to successful preservation. In this study we have evaluated the relationship between the effect of inhalation of nitric oxide and the degree of endothelial dysfunction after lung transplantation. METHODS: A left lung, which had been preserved for 24 hours, was transplanted and a right pneumonectomy was performed in 5 pigs. After a 24-hour observation period the pigs inhaled 5, 20, and 80 ppm nitric oxide, and pulmonary vascular resistance was recorded continuously. From the same donors preserved pulmonary arteries from the contralateral lung were studied simultaneously in organ baths. Acetylcholine chloride was used to elicit endothelium-dependent... (More)
BACKGROUND: Maintaining endothelial function within transplanted organs may be critical to successful preservation. In this study we have evaluated the relationship between the effect of inhalation of nitric oxide and the degree of endothelial dysfunction after lung transplantation. METHODS: A left lung, which had been preserved for 24 hours, was transplanted and a right pneumonectomy was performed in 5 pigs. After a 24-hour observation period the pigs inhaled 5, 20, and 80 ppm nitric oxide, and pulmonary vascular resistance was recorded continuously. From the same donors preserved pulmonary arteries from the contralateral lung were studied simultaneously in organ baths. Acetylcholine chloride was used to elicit endothelium-dependent relaxation in vessel segments contracted with the thromboxane A2 analogue U-46619. RESULTS: Maximal endothelium-dependent relaxation decreased in the preserved lungs and correlated to the pulmonary vascular resistance in the simultaneously transplanted lungs. Inhalation of nitric oxide in the pigs that had received transplants caused the pulmonary vessels to dilate in proportion to the endothelial dysfunction. CONCLUSIONS: Preservation of lung for transplantation induces an endothelial dysfunction, and the degree of the decrease in pulmonary vascular resistance caused by nitric oxide inhalation may be an indication of the degree of this endothelial damage. The vasodilation caused by inhaled nitric oxide increases as the endothelial function deteriorates. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Annals of Thoracic Surgery
volume
62
issue
6
pages
1639 - 1643
publisher
Elsevier
external identifiers
  • pmid:8957365
  • scopus:0030550264
ISSN
1552-6259
language
English
LU publication?
yes
id
c4b391e8-ed7a-4de7-99a1-788f385f347e (old id 1111008)
alternative location
http://ats.ctsnetjournals.org/cgi/content/full/62/6/1639
date added to LUP
2008-07-25 15:39:15
date last changed
2017-01-01 05:08:12
@article{c4b391e8-ed7a-4de7-99a1-788f385f347e,
  abstract     = {BACKGROUND: Maintaining endothelial function within transplanted organs may be critical to successful preservation. In this study we have evaluated the relationship between the effect of inhalation of nitric oxide and the degree of endothelial dysfunction after lung transplantation. METHODS: A left lung, which had been preserved for 24 hours, was transplanted and a right pneumonectomy was performed in 5 pigs. After a 24-hour observation period the pigs inhaled 5, 20, and 80 ppm nitric oxide, and pulmonary vascular resistance was recorded continuously. From the same donors preserved pulmonary arteries from the contralateral lung were studied simultaneously in organ baths. Acetylcholine chloride was used to elicit endothelium-dependent relaxation in vessel segments contracted with the thromboxane A2 analogue U-46619. RESULTS: Maximal endothelium-dependent relaxation decreased in the preserved lungs and correlated to the pulmonary vascular resistance in the simultaneously transplanted lungs. Inhalation of nitric oxide in the pigs that had received transplants caused the pulmonary vessels to dilate in proportion to the endothelial dysfunction. CONCLUSIONS: Preservation of lung for transplantation induces an endothelial dysfunction, and the degree of the decrease in pulmonary vascular resistance caused by nitric oxide inhalation may be an indication of the degree of this endothelial damage. The vasodilation caused by inhaled nitric oxide increases as the endothelial function deteriorates.},
  author       = {Lindberg, Lars and Kimblad, Per Ola and Sjöberg, Trygve and Ingemansson, Richard and Steen, Stig},
  issn         = {1552-6259},
  language     = {eng},
  number       = {6},
  pages        = {1639--1643},
  publisher    = {Elsevier},
  series       = {Annals of Thoracic Surgery},
  title        = {Inhaled nitric oxide reveals and attenuates endothelial dysfunction after lung transplantation},
  volume       = {62},
  year         = {1996},
}