Vincristine reduces damage of the blood-brain barrier induced by high intravascular pressure.
A reversible opening of the structural blood-brain barrier (BBB) was accomplished in rats by rapidly increasing the hydrostatic pressure either through forced intracarotid infusion of autologous blood or i.v. administration of angiotensin, whose effect was exaggerated by previous injection of the vasodilator, papaverine. The extent of barrier damage was evaluated in terms of the extravasation of Evans blue-albumin complex or the brain uptake of circulating [14C]inulin. Pretreatment of the animals with the antimitotic agent, vincristine, significantly reduced the barrier damage. This is interpreted as an effect of vincristine on intracellular microtubule systems, which may be involved in the vesicular transport across the endothelial cells of brain microvessels.
D000804:Angiotensin II; D000818:Animals; D001812:Blood-Brain Barrier; D001927:Brain Diseases / Q000517:prevention & control*; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014750:Vincristine / Q000627:therapeutic use*
D000804:Angiotensin II; D014750:Vincristine