Lung inflammation and hyperreactivity are often associated with a range of lung disorders including asthma and ozone-induced lung damage. As part of our model of ODTS we have investigated these phenomena in order to determine whether there is a direct link between inflammation and bronchial reactivity.

Endotoxin induced hyperreactivity to methacholine 1h post-exposure in the guinea pig. At 4h post-exposure, the hyperreactivity was no longer present. At 24 and 48h, the lungs were hyporeactive to methacholine. At 72h the lungs had returned to normal.

Reactivity to the thromboxane A2 analogue, U46619 was significantly increased at 1, 4 and 24h after endotoxin exposure. At 48h some hyperreactivity still appeared to be present, although this was not significant when compared to controls. At 72h lung reactivity to U46619 closely matched that of control animals.

Hyperreactivity to 5HT occurred at 1h post-endotoxin. However, at 72h the lungs were hyporeactive.

The number of neutrophils in the bronchoalveolar lavage fluid had significantly increased at 1h post-endotoxin exposure, but did not reach maximum levels until 4h. Over the rest of the observed period the numbers steadily declined.

Macrophage numbers began to increase at 4h post-endotoxin exposure, but did not become significantly elevated until 24h. Over the next 47h the numbers steadily declined.

There was no increase in eosinophil numbers, extracellular protein, surfactant, or wet:dry lung ratio, observed at any time examined after exposure to endotoxin.

Due to the differing time-courses of reactivity and cellular influx, and the fact that other inflammatory markers remained unchanged, we conclude that inflammation is not essential for the induction of hyperreactivity.