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Vol. 297, Issue 2, 479-488, May 2001
The A. C. Burton Vascular Biology Laboratory, London Health
Sciences Centre, and the Department of Pharmacology and Toxicology, The
University of Western Ontario, London, Ontario, Canada
We have previously demonstrated depressed vascular contractility in
intralobar pulmonary artery (PA) rings isolated from rats with acute
Pseudomonas pneumonia. Here we describe the role of arachidonic acid (AA) metabolites in the regulation of pulmonary vascular tone in inflammation. Pneumonia was induced by intratracheal injection of P. aeruginosa organisms. Rats were
sacrificed 44 h later. EETs and 20-HETE were formed at
significantly lower rates in pneumonia compared with control lung
microsomes. Vasoactive effects of CYP metabolites (5,6-EET, 8,9-EET,
11,12-EET, 14,15-EET, and 20-HETE) on small PA rings from control or
pneumonia rats were assessed in vitro. All four EETs and 20-HETE were
more potent PA vasoconstrictors than KCl or phenylephrine (PE).
However, this potency was attenuated in PA rings from pneumonia lungs
compared with control. In contrast, pneumonia had no effect on COX
activity [total pulmonary prostaglandin (PG), PGE2, and
6-keto-PGF1
]. In vitro vascular contractility to KCl,
PE, or PGF2 was assessed in small PA rings from control
and pneumonia rats in the presence and absence of the COX-2 inhibitor
NS-398 (10 µM). NS-398 did not reverse the attenuated contractile
responses to KCl, PE, or PGF2 in pneumonia rats.
Nitrite/nitrate levels, inducible nitric-oxide synthase and heme
oxygenase activities were all significantly elevated in pneumonia
lungs. In conclusion, vasodilator PGs produced by COX-2 do not
contribute to the depressed PA contractility in this model of
pneumonia. Depressed pulmonary production and vasoconstrictor effects
of CYP metabolites of AA (possibly due to increased NO and/or carbon
monoxide) indicate a potential role for these vasoactive metabolites in
this model of acute pneumonia.
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