Data on the existence of undirectional transports both ways, have accumulater in our laboratory and in the recent literature. They will be reviewed in this paper. It remains for future studies to assess the exact importance of these transport mechanisms, and of the true permeability factors (i.e. passive restriction to diffusion) for the total bloodbrain barrier effect.
An experimental procedure has been elaborated to facilitate selective effects exerted by agents applied within the cerebral vessels on EEG and blood‐brain barrier phenomena. In rabbits short‐term (less than 1 minute) perfusion of one hemisphere is performed via the ipsilateral internal carotid artery with a pressure adjusted so as to obtain displacement of the blood. This displacement is controlled by inspection of the pial vessels through a trephine opening. The technique implies control of the active concentration in loco of the applied agents and of the application time, hence graded influences near the threshold levels can be obtained.
Structural and metabolic considerations make it conceivable that low grade damage of the blood‐brain barrier may be produced with no significant effect on the neuronal activity as reflected in EEG (except for the brief influence from the blood deprivation). After such damage intravenous administration of suitable substances, unable to pass the intact barrier, may give rise to unilateral EEG changes and thus reveal the defective barrier function. Two model experiments are reported. The first one shows that unilateral blood deprivation per se (for about 2 min) exerts a marked but reversible effect on the EEG without damage to the blood‐brain barrier as tested by intravenously injected trypan blue. The second experiment illustrates an attempt to induce barrier damage without significant changes in the EEG.
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