ABSTRACT
With serotonin, cerebral blood flow decreased to a great degree during multiple injections. Serotonin was found to produce different effects on brain arterial vessels. It enhanced the resistance of carotid arteries to a greater degree than that in the cerebrobasilar system. Serotonin constricted pial arterioles with an initial diameter of more than 40 nm, whereas the microvessels of less diameter got substantially dilated. The agent had a depriming effect on somatosympathetic and vasomotor reflexes via its interaction with central noradrenergic structures.
Subject(s)
Cerebral Arteries/drug effects , Cerebral Veins/drug effects , Serotonin/pharmacology , Animals , Cats , Cerebrovascular Circulation/drug effects , Plethysmography, Impedance , Rabbits , Rats , Vascular Resistance/drug effectsABSTRACT
The cerebroprotective effect of flunarizine was studied using the following methods: hypobaric hypoxia in mice, complete ischemia by decapitation in mice, anoxic hypoxia in mice, hemic hypoxia in rats, incomplete ischemia by bilateral carotid ligation in rats and asphyxic hypoxia in cats. Piracetam, meclofenoxate, nicergoline, naftidrofuryl, cinnarizine and nifedipine were studied as reference drugs. Flunarizine increased the survival time in all survival models. Its effect was most pronounced in complete ischemia model, and considerably higher than that of reference drugs. In asphyxic hypoxia flunarizine increased cortical resistance and shortened cortical recovery. The EEG frequency-amplitude analysis during asphyxic hypoxia showed a significant decrease of the slow-waves amplitudes of delta and theta range, and an increase of the fast-waves amplitudes of beta-2 range, changes indicating protective action.
Subject(s)
Brain Ischemia/drug therapy , Flunarizine/therapeutic use , Hypoxia, Brain/drug therapy , Animals , Brain/drug effects , Carotid Arteries/physiology , Cats , Female , Flunarizine/pharmacology , Hypoxia/drug therapy , Hypoxia/mortality , Hypoxia, Brain/mortality , Male , Mice , Rats , Rats, Inbred StrainsABSTRACT
The effect of nicergoline on cerebral blood flow (CBF), cerebrovascular resistance, the constriction of cerebral vessels caused reflectorily or by 5-hydroxytryptamine (5-HT) and on the transport of 5-HT in rat brain synaptosomes was studied using different experimental models. Nicergoline reduced cerebrovascular resistance in the carotid and vertebrobasilar system. The drug decreased carotid blood flow and local cortical CBF, preceded in some experiments by short-lasting CBF increase. Nicergoline almost completely inhibited brain vessels responses in the carotid and vertebrobasilar systems after tibial nerve stimulation. Simultaneously, inhibition of reflectory discharges of the sympathetic nerves was observed. Nicergoline showed an antiserotonin action by antagonizing the 5-HT effect on the cerebral circulation and inhibiting 5-HT-induced constriction of isolated rabbit basilar artery. The inhibition of uptake and enhancement of the release of 5-HT from brain synaptosomes indicates its ability to affect neuronal transmission in serotoninergic neurons. The effects of nicergoline are probably involved in the realization of its antimigraine action.
