Hardebo J E, Nilsson B
Brain Res. 1980 Jan 6;181(1):49-59. doi: 10.1016/0006-8993(80)91258-5.
The intracarotid infusion of hyperosmolar aqueous solutions such as urea is widely used to transiently open the blood-brain barrier in various animal species. In the present study in the rat an attempt was made to analyze the hemodynamic changes caused by the intracarotid infusions with special reference to possible mechanisms underlying the barrier opening. The cerebral blood flow (as reflected by the cerebral venous outflow rate) intracranial pressure, intracarotid pressure and systemic blood pressure were continuously measured during and following the infusions. It was found that intracarotid infusions of hyperosomolar solutions induce cerebral vasodilation and flow increase. Autoregulation is impaired. Probably, a direct vasodilator mechanism is involved but, depending on volume and osmolarity of the solution used, the changes may be heavily influenced by vascular distention due to intracarotid pressure effect, and by systemic pressure changes. These mechanisms are in common with other methods for barrier opening. The local vasomotor and systemic effects of a hyperosmolar solution of urea, capable of opening the barrier, are not normalized until about 6 min after the administration.