Terbutaline and budesonide as inhibitors of postischaemic permeability increase.

A temporary ischaemia with total circulatory arrest of the hamster cheek pouch was obtained by clamping the neck of the everted cheek pouch. The macromolecular permeability increase in postcapillary venules was quantified as the leakage of fluorescein-labelled dextran using intravital microscopy and a fluorometer simultaneously. At reperfusion after 30 min ischaemia, there was a significant and reversible permeability increase. This response could be totally prevented by topical administration of either terbutaline, a selective beta 2-receptor agonist, or budesonide, a glucocorticoid, but it was not significantly impeded by the antihistamine mepyramine. The study shows that, in conformity with the situation in inflammation, the postischaemic permeability increase at reperfusion after ischaemia can be blocked by either beta 2-stimulation or glucocorticoids. Furthermore, it indicates that histamine, a common inflammatory mediator, is not responsible for the postischaemic permeability increase.