Dynamics of experimental vasogenic brain oedema in the rat: changes induced by adrenergic drugs

1 The effects of adrenergic drugs on the formation and resolution of cerebr al oedema in a rat model of cold-induced vasogenic brain oedema were studie d. Evans blue dye extravasation, water content and ultrastructural alterati ons (pinocytotic vesicle formation in capillary endothelial cells and appar ent water accumulation in the brain parenchyma) were evaluated in parietal cortex. 2 Previous administration of the alpha-adrenoceptor antagonist phenoxybenza mine produced a reduction of Evans blue extravasation and water content, di minished vesicle formation and reduced water accumulation. Previous adminis tration of the beta(2)-adrenoceptor agonist clenbuterol reduced Evans blue extravasation and water content, but did not change vesicle frequency. 3 The effects of clenbuterol on Evans blue passage to the brain were blocke d by timolol (beta-adrenoceptor antagonist) but not by metoprolol (selectiv e beta(1)-adrenoceptor antagonist). When given after the application of col d, clenbuterol was also able to reduce Evans blue and water content in the brain. Isoprenaline (beta-adrenoceptor agonist that doer not cross the bloo d-brain barrier) showed a reduction in Evans blue extravasation only when g iven intracerebroventricularly. Vinblastine (a drug that prevents vesicle f ormation) produced a reduction of the amount of pinocytotic vesicles. 4 We conclude that there is an influence of the central adrenergic nervous system on the formation and/or resolution of vasogenic brain oedema and tha t the alterations on water movement and Evans blue transport mediated by ad renergic, drugs seem ro be due, at least in part, to alterations of pinocyt otic activity in capillary endothelial cells.