Pulmonary artery contractility in pneumonia: Role of cyclooxygenase products and nitric oxide

The purpose of this study was to determine the effects of aminoguanidine (A G) and meclofenamate (MEC) on depressed contractility of small pulmonary ar tery (PA) rings isolated from a rat model of acute Pseudomonas pneumonia. C ontractility of PA rings from lungs of control or pneumonia rats was assess ed in vitro by obtaining cumulative concentration-contraction curves to pot assium chloride (KCI), phenylephrine (PE), and prostaglandin F-2 alpha (PGF (2 alpha)) on rings treated with or without MEC (1.0 mu M), AG (100 mu M), or AG + MEG. Vessels from pneumonia rats exhibited significant attenuation of the contractile responses to KCI, PE, and PGF(2 alpha). MEC restored the KCI and PGF(2 alpha) contractile responses to control values, but had no e ffect on the attenuated PE contractile response. In contrast, AG restored t he PE contractile response, and only partially affected contractile respons es to KCI and PGF(2 alpha), MEC + AG restored the contractile responses of all three agonists. We conclude that both excess nitric oxide (NO) and cycl ooxygenase products contribute to the depressed pulmonary vascular contract ility observed in rats with acute pneumonia. The relative importance of NO and cyclooxygenase products in this phenomenon depends on the contractile a gonist studied.