Ketoprofen and Phenylbutazone Attenuation of PAF-induced Lung Inflammation in Calves
The purposes of this study were: (1) to investigate which arachidonic acid metabolites contributed to platelet-activating factor (PAF) induced pulmonary dysfunction; and (2) to compare the effect of two non-steroidal anti-inflammatory drugs, phenylbutazone and ketoprofen in a model of PAF-induced re...
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Published in | The veterinary journal (1997) Vol. 157; no. 1; pp. 39 - 49 |
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Main Authors | , , , , |
Format | Journal Article Web Resource |
Language | English |
Published |
England
Elsevier Ltd
01.01.1999
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | The purposes of this study were: (1) to investigate which arachidonic acid metabolites contributed to platelet-activating factor (PAF) induced pulmonary dysfunction; and (2) to compare the effect of two non-steroidal anti-inflammatory drugs, phenylbutazone and ketoprofen in a model of PAF-induced reversible lung inflammation in six calves.
In placebo and phenylbutazone groups, PAF infusion induced significant dysfunctions in the pattern of breathing, mechanics of breathing and gas exchange. These dysfunctions were prevented by ketoprofen pretreatment, except for the mechanics of breathing which was moderately but significantly altered by the PAF challenge. In all calves, leukotriene (LT) B4plasma concentrations did not significantly increase above baseline values at any time. Prostaglandin (PG) E2plasma concentrations showed a minor significant increase in phenylbutazone pretreated calves (55.8∓25.8pg/mL from 36.7∓16.13pg/mL). Thromboxane (TX) B2plasma concentration was significantly increased during PAF challenge in placebo- and phenylbutazone-pretreated groups, but not in ketoprofen-pretreated calves (1580.0∓1370 from 42.7∓10.7pg/mL; 2340∓477 from 63∓32pg/mL; and 36.5∓4.12 from 39.3∓12.0pg/mL, respectively).
These data suggest that TXA2is an important cyclooxygenase metabolite of arachidonic acid produced in response to PAF and that ketoprofen (intramuscular injection, 3mg/kg) is more effective than phenylbutazone (intramuscular injection, 10mg/kg) in preventing respiratory dysfunctions induced by the PAF challenge 30min after drug administration. Ketoprofen did not suppress totally the PAF-induced changes in mechanics of breathing, which suggests that PAF or a secondary release of mediators could have a direct action on airway smooth muscle. |
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Bibliography: | scopus-id:2-s2.0-0033010016 |
ISSN: | 1090-0233 1532-2971 1532-2971 |
DOI: | 10.1053/tvjl.1998.8027 |