Effect of dazoxiben, a specific inhibitor of thromboxane synthetase, on acute pulmonary responses to E. coli endotoxin in anaesthetized cats.

HA Ball, J. Parratt, IJ Zeitlin

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

1 The effects of acute pretreatment with the thromboxane synthetase inhibitor dazoxiben 5 mg/kg intravenously (UK 37248‐01) were examined on the acute pulmonary responses of pentobarbitone‐anaesthetized cats to E. coli endotoxin 2 mg/kg intravenously. 2 E. coli endotoxin in control, untreated, cats resulted in a marked pulmonary hypertension, an increase in intra‐tracheal pressure (at a constant pulmonary inflation volume), an increase in both pulmonary arterial and aortic concentrations of thromboxane B2 (TXB2) and a reduction in systematic arterial PO2. 3 Dazoxiben prevented, or markedly reduced, the endotoxin‐ induced pulmonary release of TXB2, the decrease in systematic arterial PO2 and the pulmonary arterial hypertension, but did not modify the increase in intratracheal pressure. 4 These results may suggest that TXA2 is responsible for the endotoxin‐induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin. 1983 The British Pharmacological Society

Original languageEnglish
Pages (from-to)127S-131S
JournalBritish Journal of Clinical Pharmacology
Volume15
Issue number1 S
DOIs
Publication statusPublished - 1983

Fingerprint

Thromboxane-A Synthase
Endotoxins
Cats
Pulmonary Hypertension
Escherichia coli
Lung
Thromboxane B2
Lung Compliance
Pressure
Dinoprost
Economic Inflation
Arachidonic Acid
dazoxiben

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

@article{bd1120da8f4e499c86782fb40df0be17,
title = "Effect of dazoxiben, a specific inhibitor of thromboxane synthetase, on acute pulmonary responses to E. coli endotoxin in anaesthetized cats.",
abstract = "1 The effects of acute pretreatment with the thromboxane synthetase inhibitor dazoxiben 5 mg/kg intravenously (UK 37248‐01) were examined on the acute pulmonary responses of pentobarbitone‐anaesthetized cats to E. coli endotoxin 2 mg/kg intravenously. 2 E. coli endotoxin in control, untreated, cats resulted in a marked pulmonary hypertension, an increase in intra‐tracheal pressure (at a constant pulmonary inflation volume), an increase in both pulmonary arterial and aortic concentrations of thromboxane B2 (TXB2) and a reduction in systematic arterial PO2. 3 Dazoxiben prevented, or markedly reduced, the endotoxin‐ induced pulmonary release of TXB2, the decrease in systematic arterial PO2 and the pulmonary arterial hypertension, but did not modify the increase in intratracheal pressure. 4 These results may suggest that TXA2 is responsible for the endotoxin‐induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin. 1983 The British Pharmacological Society",
author = "HA Ball and J. Parratt and IJ Zeitlin",
year = "1983",
doi = "10.1111/j.1365-2125.1983.tb02123.x",
language = "English",
volume = "15",
pages = "127S--131S",
journal = "British Journal of Clinical Pharmacology",
issn = "0306-5251",
publisher = "Wiley-Blackwell",
number = "1 S",

}

TY - JOUR

T1 - Effect of dazoxiben, a specific inhibitor of thromboxane synthetase, on acute pulmonary responses to E. coli endotoxin in anaesthetized cats.

AU - Ball, HA

AU - Parratt, J.

AU - Zeitlin, IJ

PY - 1983

Y1 - 1983

N2 - 1 The effects of acute pretreatment with the thromboxane synthetase inhibitor dazoxiben 5 mg/kg intravenously (UK 37248‐01) were examined on the acute pulmonary responses of pentobarbitone‐anaesthetized cats to E. coli endotoxin 2 mg/kg intravenously. 2 E. coli endotoxin in control, untreated, cats resulted in a marked pulmonary hypertension, an increase in intra‐tracheal pressure (at a constant pulmonary inflation volume), an increase in both pulmonary arterial and aortic concentrations of thromboxane B2 (TXB2) and a reduction in systematic arterial PO2. 3 Dazoxiben prevented, or markedly reduced, the endotoxin‐ induced pulmonary release of TXB2, the decrease in systematic arterial PO2 and the pulmonary arterial hypertension, but did not modify the increase in intratracheal pressure. 4 These results may suggest that TXA2 is responsible for the endotoxin‐induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin. 1983 The British Pharmacological Society

AB - 1 The effects of acute pretreatment with the thromboxane synthetase inhibitor dazoxiben 5 mg/kg intravenously (UK 37248‐01) were examined on the acute pulmonary responses of pentobarbitone‐anaesthetized cats to E. coli endotoxin 2 mg/kg intravenously. 2 E. coli endotoxin in control, untreated, cats resulted in a marked pulmonary hypertension, an increase in intra‐tracheal pressure (at a constant pulmonary inflation volume), an increase in both pulmonary arterial and aortic concentrations of thromboxane B2 (TXB2) and a reduction in systematic arterial PO2. 3 Dazoxiben prevented, or markedly reduced, the endotoxin‐ induced pulmonary release of TXB2, the decrease in systematic arterial PO2 and the pulmonary arterial hypertension, but did not modify the increase in intratracheal pressure. 4 These results may suggest that TXA2 is responsible for the endotoxin‐induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin. 1983 The British Pharmacological Society

UR - http://www.scopus.com/inward/record.url?scp=0020581331&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020581331&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2125.1983.tb02123.x

DO - 10.1111/j.1365-2125.1983.tb02123.x

M3 - Article

C2 - 6337603

AN - SCOPUS:0020581331

VL - 15

SP - 127S-131S

JO - British Journal of Clinical Pharmacology

JF - British Journal of Clinical Pharmacology

SN - 0306-5251

IS - 1 S

ER -