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Am. J. Respir. Crit. Care Med., Volume 156, Number 2, August 1997, 654-658

In Vivo Treatment with Endotoxin Increases Rat Pulmonary Vascular Contractility Despite NOS Induction

MARK J. D. GRIFFITHS, NICHOLAS P. CURZEN, JANE A. MITCHELL, and TIMOTHY W. EVANS

Unit of Critical Care, Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom

Pulmonary hypertension is a feature of clinical and experimental acute lung injury. Nitric oxide (NO) synthesis is increased in hyporesponsive systemic and pulmonary conductance arteries after endotoxin (LPS) injection in the rat. We examined the effects of NO synthase (NOS) induction by LPS on vascular reactivity of the isolated perfused rat lung (IPL) using the selective inducible (iNOS) inhibitor aminoguanidine (AG). Baseline pulmonary artery pressures (Ppa) were higher in the LPS compared with the sham-treated rats and were further increased only in the LPS-treated group by AG. Increased NOS activity in whole lung and the vasopressor effect of AG suggested that iNOS was active in pulmonary resistance vessels after LPS treatment. Vasoconstriction to hypoxia, angiotensin II (AII), and prostaglandin F2alpha (PGF2alpha ) was enhanced or unchanged in LPS-treated rats despite NOS induction. Hence, iNOS activity counterbalances increased pulmonary vascular contractility in this model.




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