Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells

T. Tanita, S. Ueda, S. Ono, Yasushi Hoshikawa, T. Tabata, M. Noda, S. Suzuki, M. Chida, Y. Ashino, S. Fujimura

Research output: Contribution to journalArticle

Abstract

To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These data indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

Original languageEnglish
Pages (from-to)1093-1098
Number of pages6
JournalJapanese Journal of Thoracic Diseases
Volume33
Issue number10
Publication statusPublished - 01-01-1995

Fingerprint

Capillary Permeability
Prostaglandin-Endoperoxide Synthases
Leukocytes
Lung
Meclofenamic Acid
Cyclooxygenase Inhibitors
Vascular Resistance
Blood Vessels
Vascular System Injuries
Vascular Endothelium
Lung Injury
Glass
Sprague Dawley Rats
Perfusion

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

Tanita, T. ; Ueda, S. ; Ono, S. ; Hoshikawa, Yasushi ; Tabata, T. ; Noda, M. ; Suzuki, S. ; Chida, M. ; Ashino, Y. ; Fujimura, S. / Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells. In: Japanese Journal of Thoracic Diseases. 1995 ; Vol. 33, No. 10. pp. 1093-1098.
@article{f59e3565cc1b4368880cb7723d4241f6,
title = "Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells",
abstract = "To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These data indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.",
author = "T. Tanita and S. Ueda and S. Ono and Yasushi Hoshikawa and T. Tabata and M. Noda and S. Suzuki and M. Chida and Y. Ashino and S. Fujimura",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "33",
pages = "1093--1098",
journal = "Respiratory Investigation",
issn = "2212-5345",
publisher = "Elsevier BV",
number = "10",

}

Tanita, T, Ueda, S, Ono, S, Hoshikawa, Y, Tabata, T, Noda, M, Suzuki, S, Chida, M, Ashino, Y & Fujimura, S 1995, 'Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells', Japanese Journal of Thoracic Diseases, vol. 33, no. 10, pp. 1093-1098.

Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells. / Tanita, T.; Ueda, S.; Ono, S.; Hoshikawa, Yasushi; Tabata, T.; Noda, M.; Suzuki, S.; Chida, M.; Ashino, Y.; Fujimura, S.

In: Japanese Journal of Thoracic Diseases, Vol. 33, No. 10, 01.01.1995, p. 1093-1098.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells

AU - Tanita, T.

AU - Ueda, S.

AU - Ono, S.

AU - Hoshikawa, Yasushi

AU - Tabata, T.

AU - Noda, M.

AU - Suzuki, S.

AU - Chida, M.

AU - Ashino, Y.

AU - Fujimura, S.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These data indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

AB - To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These data indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

UR - http://www.scopus.com/inward/record.url?scp=0028880503&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028880503&partnerID=8YFLogxK

M3 - Article

C2 - 8544381

AN - SCOPUS:0028880503

VL - 33

SP - 1093

EP - 1098

JO - Respiratory Investigation

JF - Respiratory Investigation

SN - 2212-5345

IS - 10

ER -