Kawamura S, Yasui N
Department of Surgical Neurology, Research Institute for Brain, Akita.
Neurol Med Chir (Tokyo). 1994 Oct;34(10):663-7. doi: 10.2176/nmc.34.663.
The effects of the Ca2+ entry blocker nilvadipine on the diameter of the brain surface microvessels of rats were studied in vivo using intravital fluorescence microscopy and a closed cranial window technique under an intracranial pressure of 5-7 mmHg. Intravenous Na(+)-fluorescein was used as a blood-brain barrier (BBB) and vessel marker. The BBB function, as determined by the barrier marker, remained intact during the entire observation period. Nilvadipine (10(-10)-10(-6)M) and/or vehicle were dissolved in artificial cerebrospinal fluid (CSF). Superfusion of the brain surface with artificial CSF with and without vehicle had no effect on vessel diameters. Nilvadipine dilated pial arterioles in a dose-dependent manner. The arterioles were dilated significantly at concentrations of > or = 10(-9)M when compared with resting diameters. The diameters of venules were not affected by nilvadipine. The results suggest a possible mechanism for the nilvadipine-induced increase in the cerebral blood flow under physiological conditions.
