Disparate IL-1β and iNOS gene expression in the aorta and pulmonary artery after endotoxemia

Ben M. Tsai, Meijing Wang, Jeffrey M. Pitcher, Ajay Kher, Daniel R. Meldrum

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Background: Endotoxemia causes paradoxical effects on the systemic and pulmonary vasculature, resulting in systemic hypotension and increased pulmonary artery pressure. The local production of inflammatory mediators may have important effects on vascular tissue function. The purpose of this study was to delineate differences in function and the expression of tissue cytokine genes in the aorta and pulmonary artery after endotoxemia. Methods: Thoracic aorta and pulmonary artery branches were isolated from adult Sprague-Dawley rats (n = 4-6/group) 6 h after intraperitoneal injection of lipopolysaccharide (Salmonella typhimurium, 20 mg/kg) or vehicle (1.0 mL of saline). Arteries were suspended in perfused organ baths for measurement of isometric force transduction, and dose-response curves to phenylephrine (0.01-10 micromol/L), acetylcholine (0.01-10 micromol/L), and sodium nitroprusside (0.001-10 micromol/L) were generated. The vascular segments were also assessed for expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) by semiquantitative reverse transcriptase-polymerase chain reaction. Results: Endotoxemia resulted in decreased contractility of the aorta (508.63 ± 81.89 mg vs. 2544.16 ± 142.05 mg in the vehicle group) and pulmonary artery (352.50 ± 38.11 mg vs. 535.83 ± 45.51 mg in the vehicle group) and decreased endothelium-dependent pulmonary artery relaxation (52.86 ± 5.63% vs. 80.58 ± 6.39% in the vehicle group). Expression of IL-1β and iNOS mRNA by the pulmonary artery, but not the aorta, increased significantly in the endotoxin-treated animals. Interleukin-6 was increased in both the pulmonary artery and the aorta during endotoxemia, whereas TNF concentrations were unchanged. Conclusions: Endotoxemia may cause aortic hypocontractility and impaired endothelium-dependent pulmonary artery vasorelaxation. Expression of inflammatory genes in vascular tissue may be site-specific and may contribute to the functional derangements associated with sepsis.

Original languageEnglish
Pages (from-to)21-27
Number of pages7
JournalSurgical Infections
Volume7
Issue number1
DOIs
StatePublished - Feb 2006

Fingerprint

Endotoxemia
Nitric Oxide Synthase Type II
Interleukin-1
Pulmonary Artery
Aorta
Gene Expression
Blood Vessels
Endothelium
Interleukin-6
Thoracic Arteries
Messenger RNA
Nitroprusside
Phenylephrine
Salmonella typhimurium
Intraperitoneal Injections
Reverse Transcriptase Polymerase Chain Reaction
Thoracic Aorta
Baths
Endotoxins
Vasodilation

ASJC Scopus subject areas

  • Surgery
  • Microbiology (medical)

Cite this

Disparate IL-1β and iNOS gene expression in the aorta and pulmonary artery after endotoxemia. / Tsai, Ben M.; Wang, Meijing; Pitcher, Jeffrey M.; Kher, Ajay; Meldrum, Daniel R.

In: Surgical Infections, Vol. 7, No. 1, 02.2006, p. 21-27.

Research output: Contribution to journalArticle

Tsai, Ben M. ; Wang, Meijing ; Pitcher, Jeffrey M. ; Kher, Ajay ; Meldrum, Daniel R. / Disparate IL-1β and iNOS gene expression in the aorta and pulmonary artery after endotoxemia. In: Surgical Infections. 2006 ; Vol. 7, No. 1. pp. 21-27.
@article{516d1682a7c842a3bcbdf03072ec7c07,
title = "Disparate IL-1β and iNOS gene expression in the aorta and pulmonary artery after endotoxemia",
abstract = "Background: Endotoxemia causes paradoxical effects on the systemic and pulmonary vasculature, resulting in systemic hypotension and increased pulmonary artery pressure. The local production of inflammatory mediators may have important effects on vascular tissue function. The purpose of this study was to delineate differences in function and the expression of tissue cytokine genes in the aorta and pulmonary artery after endotoxemia. Methods: Thoracic aorta and pulmonary artery branches were isolated from adult Sprague-Dawley rats (n = 4-6/group) 6 h after intraperitoneal injection of lipopolysaccharide (Salmonella typhimurium, 20 mg/kg) or vehicle (1.0 mL of saline). Arteries were suspended in perfused organ baths for measurement of isometric force transduction, and dose-response curves to phenylephrine (0.01-10 micromol/L), acetylcholine (0.01-10 micromol/L), and sodium nitroprusside (0.001-10 micromol/L) were generated. The vascular segments were also assessed for expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) by semiquantitative reverse transcriptase-polymerase chain reaction. Results: Endotoxemia resulted in decreased contractility of the aorta (508.63 ± 81.89 mg vs. 2544.16 ± 142.05 mg in the vehicle group) and pulmonary artery (352.50 ± 38.11 mg vs. 535.83 ± 45.51 mg in the vehicle group) and decreased endothelium-dependent pulmonary artery relaxation (52.86 ± 5.63{\%} vs. 80.58 ± 6.39{\%} in the vehicle group). Expression of IL-1β and iNOS mRNA by the pulmonary artery, but not the aorta, increased significantly in the endotoxin-treated animals. Interleukin-6 was increased in both the pulmonary artery and the aorta during endotoxemia, whereas TNF concentrations were unchanged. Conclusions: Endotoxemia may cause aortic hypocontractility and impaired endothelium-dependent pulmonary artery vasorelaxation. Expression of inflammatory genes in vascular tissue may be site-specific and may contribute to the functional derangements associated with sepsis.",
author = "Tsai, {Ben M.} and Meijing Wang and Pitcher, {Jeffrey M.} and Ajay Kher and Meldrum, {Daniel R.}",
year = "2006",
month = "2",
doi = "10.1089/sur.2006.7.21",
language = "English",
volume = "7",
pages = "21--27",
journal = "Surgical Infections",
issn = "1096-2964",
publisher = "Mary Ann Liebert Inc.",
number = "1",

}

TY - JOUR

T1 - Disparate IL-1β and iNOS gene expression in the aorta and pulmonary artery after endotoxemia

AU - Tsai, Ben M.

AU - Wang, Meijing

AU - Pitcher, Jeffrey M.

AU - Kher, Ajay

AU - Meldrum, Daniel R.

PY - 2006/2

Y1 - 2006/2

N2 - Background: Endotoxemia causes paradoxical effects on the systemic and pulmonary vasculature, resulting in systemic hypotension and increased pulmonary artery pressure. The local production of inflammatory mediators may have important effects on vascular tissue function. The purpose of this study was to delineate differences in function and the expression of tissue cytokine genes in the aorta and pulmonary artery after endotoxemia. Methods: Thoracic aorta and pulmonary artery branches were isolated from adult Sprague-Dawley rats (n = 4-6/group) 6 h after intraperitoneal injection of lipopolysaccharide (Salmonella typhimurium, 20 mg/kg) or vehicle (1.0 mL of saline). Arteries were suspended in perfused organ baths for measurement of isometric force transduction, and dose-response curves to phenylephrine (0.01-10 micromol/L), acetylcholine (0.01-10 micromol/L), and sodium nitroprusside (0.001-10 micromol/L) were generated. The vascular segments were also assessed for expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) by semiquantitative reverse transcriptase-polymerase chain reaction. Results: Endotoxemia resulted in decreased contractility of the aorta (508.63 ± 81.89 mg vs. 2544.16 ± 142.05 mg in the vehicle group) and pulmonary artery (352.50 ± 38.11 mg vs. 535.83 ± 45.51 mg in the vehicle group) and decreased endothelium-dependent pulmonary artery relaxation (52.86 ± 5.63% vs. 80.58 ± 6.39% in the vehicle group). Expression of IL-1β and iNOS mRNA by the pulmonary artery, but not the aorta, increased significantly in the endotoxin-treated animals. Interleukin-6 was increased in both the pulmonary artery and the aorta during endotoxemia, whereas TNF concentrations were unchanged. Conclusions: Endotoxemia may cause aortic hypocontractility and impaired endothelium-dependent pulmonary artery vasorelaxation. Expression of inflammatory genes in vascular tissue may be site-specific and may contribute to the functional derangements associated with sepsis.

AB - Background: Endotoxemia causes paradoxical effects on the systemic and pulmonary vasculature, resulting in systemic hypotension and increased pulmonary artery pressure. The local production of inflammatory mediators may have important effects on vascular tissue function. The purpose of this study was to delineate differences in function and the expression of tissue cytokine genes in the aorta and pulmonary artery after endotoxemia. Methods: Thoracic aorta and pulmonary artery branches were isolated from adult Sprague-Dawley rats (n = 4-6/group) 6 h after intraperitoneal injection of lipopolysaccharide (Salmonella typhimurium, 20 mg/kg) or vehicle (1.0 mL of saline). Arteries were suspended in perfused organ baths for measurement of isometric force transduction, and dose-response curves to phenylephrine (0.01-10 micromol/L), acetylcholine (0.01-10 micromol/L), and sodium nitroprusside (0.001-10 micromol/L) were generated. The vascular segments were also assessed for expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) by semiquantitative reverse transcriptase-polymerase chain reaction. Results: Endotoxemia resulted in decreased contractility of the aorta (508.63 ± 81.89 mg vs. 2544.16 ± 142.05 mg in the vehicle group) and pulmonary artery (352.50 ± 38.11 mg vs. 535.83 ± 45.51 mg in the vehicle group) and decreased endothelium-dependent pulmonary artery relaxation (52.86 ± 5.63% vs. 80.58 ± 6.39% in the vehicle group). Expression of IL-1β and iNOS mRNA by the pulmonary artery, but not the aorta, increased significantly in the endotoxin-treated animals. Interleukin-6 was increased in both the pulmonary artery and the aorta during endotoxemia, whereas TNF concentrations were unchanged. Conclusions: Endotoxemia may cause aortic hypocontractility and impaired endothelium-dependent pulmonary artery vasorelaxation. Expression of inflammatory genes in vascular tissue may be site-specific and may contribute to the functional derangements associated with sepsis.

UR - http://www.scopus.com/inward/record.url?scp=33645564571&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645564571&partnerID=8YFLogxK

U2 - 10.1089/sur.2006.7.21

DO - 10.1089/sur.2006.7.21

M3 - Article

C2 - 16509782

AN - SCOPUS:33645564571

VL - 7

SP - 21

EP - 27

JO - Surgical Infections

JF - Surgical Infections

SN - 1096-2964

IS - 1

ER -