Bronchoconstriction induced by intratracheal administration of platelet-activating factor (PAF-acether) in baboons

Intratracheal administration of PAF-acether (60 microgram.kg-1) was performed in six premedicated, curarized and mechanically ventilated baboons. Whereas intratracheal administration of an equal amount of solvent (200 microliter of 80 degrees alcohol in 2 ml of saline) caused no measurable changes in lung mechanics, administration of PAF-acether caused an almost immediate bronchoconstriction that was spontaneously reversible within about 30 min. The concomitant fall in platelet count in peripheral blood and reduction of perfusion of ventilated lung territories estimated from the alveolar-arterial difference in CO2 tension provide circumstantial evidence that PAF-acether also caused aggregation of platelets in the lung microcirculation. In keeping with the release of PAF-acether by human alveolar macrophages, our findings suggest that this mediator may play a role in human asthma.