[Effect of S-amlodipine nicotinate on the cerebral circulation in rats under conditions of ischemic and hemorrhagic brain injury].

We have performed a comparative study of the effects of S-amlodipine nicotinate and nimodipine on the local cerebral blood flow were studied in intact rats and those with model ischemic and hemorrhagic brain injury. It is established that S-amlodipine nicotinate produces a somewhat more pronounced enhancement of cerebral blood flow in rats with ischemic and hemorrhagic brain injury than in intact animals. In addition, S-amlodipine nicotinate significantly exceed nimodipine with respect to cerebrovascular activity in rats with brain pathology of both ischemic and hemorrhagic nature.

[Cerebrovascular pharmacology of separate and combined vascular pathology of brain and heart].

The effect of nimodipine, mexidol, melatonin, afobazole, 5-hydroxy-adanamtan-2-one, and GABA conjugates with arachidonic acid and docosahexaenoyl dopamine on the cerebral circulation has been studied in intact rats and those with global transient cerebral ischemia, experimental myocardial infarction, and combined vascular pathology of brain and heart. The most pronounced vasodilation activity in rats with global transient cerebral ischemia is exhibited by nimodipine, mexidol, melatonin, afobazole, 5-hydroxy-adanamtan-2-one, and GABA-containing lipid derivatives. This effect of all these drugs (except for nimodipine) is not manifested on the background of GABA receptor blocker bicuculline.

[Peculiarities of cerebrovascular effects of GABA conjugate with docosahexaenoyl dopamine under conditions of separate and combined vascular pathology of brain and heart].

A GABA conjugate with docosahexaenoyl dophamine (DHED) enhanced local cerebral blood flow in rats under conditions of global transient cerebral ischemia, experimental myocardial infarction, and combined vascular pathology of brain and heart. At the same time, the GABA-DHED conjugate did not influence brain hemoperfusion in intact animals. The cerebrovascular effect of this conjugate is determined by its direct action on the vascular tone, since no changes in blood pressure have been observed.

[GABAergic mechanism of the cerebrovascular effect of melatonin].

In most experiments on rats under conditions of cerebral global transient ischemia, melatonin substantially enhanced local blood flow and decreased arterial blood pressure. In intact rats, the effect of melatonin on brain perfusion was much less pronounced and the arterial pressure was not influenced at all. The mechanism of melatonin action has been studied with the aid of bicuculline.

[Influence of 2-ethyl-6-methyl-3-hydroxypyridine hemisuccinate on cerebral blood perfusion in rats under experimental pathology conditions].

Experiments on rats showed that 2-ethyl-6-methyl-3-hydroxypyridine hemisuccinate increases cerebral blood flow in the system of carotid arteries both in intact animals and under conditions of global transient ischemia. In combination with tropoxin, 2-ethyl-6-methyl-3-hydroxypyridine hemisuccinate enhances the blood flow in the inner carotid artery of intact rats and the local blood flow under conditions of global transient ischemia. A combination of 2-ethyl-6-methyl-3-hydroxypyridine hemisuccinate and tropoxin increases baseline cerebral blood flow and decreases the constrictor reaction of cerebral blood vessels to 5HT(2B/2C) receptor agonist meta-chlorophenylpiperazine.

[Afobazole effect on cerebral circulation under hemorrhagic stroke model conditions].

Narcotized rats under hemorrhagic stroke model conditions exhibit a significant decrease in the cerebral flow in the region of contralateral cerebral hemisphere symmetric to the zone of lesion. Under these conditions, afobazole produced a significant increase in the local circulation in cerebral cortex, which was violated by hemorrhagic stroke. The cerebrovascular effect of afobazole was not manifested in cases of hemorrhagic stroke on the background of GABA receptor blocking by bicuculline.

[Effects of afobazole on the stress protein HSP70 level in the brain tissue of rats with global transient ischemia].

Experiments in anesthetized rats showed that global transient brain ischemia caused a significant decrease in cerebral blood flow in rat cerebral cortex and reduced the stress protein HSP70 level in striatum. Afobazole administration restored the cerebral blood supply disturbed by ischemia and increased the stress protein HSP70 synthesis in striatum.

[Cerebrovascular and antiaggregative effects of GABA-docosahexaenoyldopamine conjugate].

The effects of GABA - docosahexaenoyldopamine (DHED) conjugate on the cerebral haemodynamics and thrombocyte aggregation were evaluated and compared to these of docosahexaenoyldopamine alone. The GABA - DHED conjugate was shown to significantly enhance the cerebral circulation in rats with a model of global transient cerebral ischemia, as compared to the intact animals. Administered alone, DHED increased the blood supply of both intact and ischemic brains to an equal extent.

[Effects of an antiischemic drug combination and nimodipine on cerebral blood supply in a hemorrhagic stroke model in rats].

Narcotized rats with a hemorrhagic stroke model demonstrate a significant decrease in the cerebral flow in the area of contralateral cerebral hemisphere symmetric to the zone of lesion. Under these conditions, an antiischemic drug combination produced a pronounced but short increase in the local circulation in cortex of cerebrum (decreased by hemorrhagic stroke), with the subsequent decrease in the local flow. Nimodipine (used as the reference drug) increased the cerebral blood flow to a lesser degree, but was superior to the tested composition with respect to the effect duration.