Journal of Applied Physiology
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J Appl Physiol 69: 1494-1501, 1990;
8750-7587/90 $5.00
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Journal of Applied Physiology, Vol 69, Issue 4 1494-1501, Copyright © 1990 by American Physiological Society

ARTICLES

Cyclooxygenase inhibition prevents PMA-induced increases in lung vascular permeability

P. B. Zanaboni, J. D. Bradley, L. J. Baudendistel, R. O. Webster and T. E. Dahms
Department of Pharmacology, St. Louis University School of Medicine, Missouri 63104.

The effect of cyclooxygenase inhibition in phorbol myristate acetate (PMA)-induced acute lung injury was studied in isolated constant-flow blood-perfused rabbit lungs. PMA caused a 51% increase in pulmonary arterial pressure (localized in the arterial and middle segments as measured by vascular occlusion pressures), a 71% increase in microvascular permeability (measured by the microvascular fluid filtration coefficient, Kf), and a nearly threefold increase in perfusate thromboxane (Tx) B2 levels. Cyclooxygenase inhibition with three chemically dissimilar inhibitors, indomethacin (10(-7) and 10(-6) M), meclofenamate (10(-6) M), and ibuprofen (10(-5) M), prevented the Kf increase without affecting the pulmonary arterial pressure increase or resistance distribution changes after PMA administration. The specific role of TxA2 was investigated by pretreatment with OKY-046, a specific Tx synthase inhibitor, or infusion of SQ 29548, a TxA2 receptor antagonist; both compounds failed to protect against either the PMA-induced permeability or the vascular resistance increase. These results indicate that cyclooxygenase-mediated products of arachidonic acid other than TxA2 mediate the PMA-induced permeability increase but not the hypertension.


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