[Morphological changes in brain tissues of rat with local permanent ischemia model under the action of 2-methyl-6-ethyl-3-hydroxypyridine hemisuccinate].

The influence of 2-methyl-6-ethyl-3-hydroxypiridine hemisuccinate on the morphological state of rat brain tissue after the occlusion of left middle cerebral artery has been studied. It was found that 6- and 12-day treatment with 2-methyl-6-ethyl-3-hydroxypyridine hemisuccinate at a dose of 100 mg/kg (intraperitoneal) led to regenerative processes in ischemic brain tissue. The latter treatment duration was most effective.

[The effect of 5-hydroxyadamantan-2-one on morphological status of rats' brain tissues in local permanent ischemia conditions].

The effect of 5-hydroxyadamantane-2-one was studied on morphological state of brain tissue of rats after the occlusion of left middle cerebral artery. It was shown that intraperitoneal administration of 5-hydroxyadamantane-2-on at dose 100mg/kg, in 30 minutes after occlusion and once daily for the following 6 and 12 days leads to significant regenerative processes in brain tissue. These processes were more profound after the 12-day treatment with 5-hydroxyadamanta-ne-2-one.

[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.

[Correlations of pharmacokinetics and pharmacodynamics of a combined preparation containing pyrrolidone and pyroglutamic acid].

Experiments showed that a new drug composition containing pyrrolidone and pyroglutamic acid exhibits a significant cerebrovascular effect upon peroral administration in rats. The pharmacokinetics of pyrrolidone monitored upon its combined administration with pyroglutamic acid shows that this drug, as a component of the composition, is characterized by a high absolute bioavailability and permeability trough the blood-brain barrier. The presence of pyroglutamic acid slows down the absorption and elimination of pyrrolidone and enhances its distribution in the organs and tissues.

[GABA reuptake by rat brain slices in hypokinesia and under the influence of cinnarizine and flunarizine].

Studies showed that 15-day restriction of motor activity inhibits the reuptake of GABA by sections of the rat brain cortex and hypothalamus. In prolonged intraperitoneal injection of 10 mg/kg cinnarizine in hyperkinesia, further inhibition of this process in hypothalamic sections is encountered on the 15th days. Flunarizin (1 mg/kg) administered in a like manner has no significant effect on GABA reuptake.

[Various aspects of increased resistance of the brain tissue and its vessels to extreme effects with the use of GABAergic compounds and Ca(2+) antagonists].

Experiments on rats showed that the morpho-functional state of the cerebral cortex microcirculatory bed suffers marked changes in different periods of hypokinesia. This was accompanied with obvious morphological changes in the brain, the development of brain edema in particular. It was found that the GABAergic agents which we used ranked below Ca-antagonists in antiedemic activity.

[The effect of calcium channel blockers on activity in the sympathetic nerves, on the vasomotor reflex and on cerebral circulation].

Experiments on cats showed that calcium canal blockers of the dihydropyridine series (nimodipine, nifedipine) and, to a lesser measure diphenylpiperazine derivatives increase the activity in sympathetic nerves attributable to the central effect of the drugs. Cinnarizine had a diametrically opposite effect. Cinnarizine, nimodipine, and nifedipine reduced the reflex pressor response of the arterial pressure, whereas flunarizine mainly promoted the vasomotor reflex.

[Cerebral blood flow and thrombocyte aggregation at different times of hypokinesia and their regulation by antiaggregants].

Changes in local cerebral blood flow and in microcirculatory channels in the cortex of rat brain were studied in conditions of early and remote hypokinesia. The rheological parameters of blood were studied in patients which stayed in ber for a long time in traumatological hospitals. We showed that by the 60th day of hypokinesia and in conditions of active readaptation the disordered cerebral blood flow starts to stabilize and tendency to normalization of some parameters of the cerebral blood flow and microcirculatory channels become clearly seen.

[The cerebral blood circulation during hypokinesia under the influence of hypercapnia, hypotonia, GABA and neurosensory stimulation].

We studied the formation of vasomotor reflexes in hypokinesia and responses of the brain vessels to the action of GABA, hypotension, and hypercapnia. We found that the response of the brain vessels to GABA is delayed and the mechanisms which supported an adequate cerebral vasculation are distorted in hypotension. At the same time the disturbance of the reflectory reaction of the brain vessels in the course of forming the vasomotor reflexes and the absence of significant changes in response to GABA were noticed.