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J Appl Physiol 74: 1117-1122, 1993;
8750-7587/93 $5.00
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Journal of Applied Physiology, Vol 74, Issue 3 1117-1122, Copyright © 1993 by American Physiological Society

ARTICLES

Effect of inhaled lyso-platelet-activating factor on airway microvascular leakage in the guinea pig

T. Sakamoto, W. Elwood, P. J. Barnes and K. F. Chung
Department of Thoracic Medicine, National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom.

Lyso-platelet-activating factor (PAF), the precursor and metabolite of PAF, is considered inactive, although it may be converted to PAF by airway cells. We have investigated the effects of inhaled lyso-PAF on bronchoconstriction and airway microvascular leakage in anesthetized guinea pigs. Lung resistance (RL) was measured for 6 min after inhalation of lyso-PAF (0.3, 1, and 3 mM; 30 breaths) followed by measurement of extravasation of intravenous Evans blue dye into airway tissues, which was used as an index of airway microvascular leakage. Inhaled lyso-PAF caused an increase in RL and leakage of dye at all airway levels in a dose-dependent fashion, but intravenous lyso-PAF (0.25 mg/kg) had no airway effect. The maximum dose of inhaled lyso-PAF increased RL significantly by approximately 200%. The amount of extravasation of dye induced was 96 +/- 4 (SE) ng/mg of tissue in trachea, 77 +/- 8 ng/mg in main bronchi, and 65 +/- 7 and 25 +/- 1 ng/mg in proximal and distal intrapulmonary airways respectively; these values were all significantly higher (P < 0.01) than control values. These responses were completely abolished by a specific PAF-receptor antagonist WEB-2086 (2 mg/kg iv). Our results show that inhaled lyso-PAF is potent in increasing airway microvascular leakage. The effects of lyso-PAF may result from its metabolic transformation to PAF by lyso-PAF:acetyl-CoA acetyltransferase in the airway.


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