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

Abstract

The effects of adrenergic drugs on the formation and resolution of cerebral oedema in a rat model of cold-induced vasogenic brain oedema were studied. Evans blue dye extravasation, water content and ultrastructural alterations (pinocytotic vesicle formation in capillary endothelial cells and apparent water accumulation in the brain parenchyma) were evaluated in parietal cortex. Previous administration of the alpha-adrenoceptor antagonist phenoxybenzamine produced a reduction of Evans blue extravasation and water content, diminished vesicle formation and reduced water accumulation. Previous administration of the beta2-adrenoceptor agonist clenbuterol reduced Evans blue extravasation and water content, but did not change vesicle frequency. The effects of clenbuterol on Evans blue passage to the brain were blocked by timolol (beta-adrenoceptor antagonist) but not by metoprolol (selective beta1-adrenoceptor antagonist). When given after the application of cold, clenbuterol was also able to reduce Evans blue and water content in the brain. Isoprenaline (beta-adrenoceptor agonist that does not cross the blood-brain barrier) showed a reduction in Evans blue extravasation only when given intracerebroventricularly. Vinblastine (a drug that prevents vesicle formation) produced a reduction of the amount of pinocytotic vesicles. We conclude that there is an influence of the central adrenergic nervous system on the formation and/or resolution of vasogenic brain oedema and that the alterations on water movement and Evans blue transport mediated by adrenergic drugs seem to be due, at least in part, to alterations of pinocytotic activity in capillary endothelial cells.

Dexmedetomidine post-treatment induces neuroprotection via activation of extracellular signal-regulated kinase in rats with subarachnoid haemorrhage

“…Dexmedetomidine might inhibit these mechanisms via its neuroprotective effects, and might also work through α 2 AR to control the BBB permeability directly. 31 These effects should contribute to dexmedetomidine-induced reduction of brain oedema after SAH as observed in the present study.…”

Glut1/SLC2A1 is crucial for the development of the blood‐brain barrier in vivo

“…The experiments are done as described elsewhere29, 30 with some modifications. In brief, the living larvae at 4 dpf were decapitated (Supplementary Fig 5) and rapidly weighed (wet weight).…”

Bolus isoproterenol infusions provide a reliable method for assessing interoceptive awareness

“…The pharmacological effects of isoproterenol are transient, owing to a short half-life in the blood (Conolly, et al, 1972), providing an opportunity for repeated administrations with reproducible effects within a single experimental session (Martinsson, Lindvall, Melcher, & Hjemdahl, 1989). Furthermore, since isoproterenol is believed to only minimally cross the blood brain barrier (Borges, Sarmento, & Azevedo, 1999; Murphy & Johanson, 1985; Olesen, Hougard, & Hertz, 1978), it is unlikely that the effects of isoproterenol administration result directly in changes in brain activity. This presents a unique opportunity to examine the effects of stimulation restricted to afferent sensory nerve fibers on interoceptive awareness and emotional experience.…”