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Microgliocytes are currently known as structurally labile cells, that, by changing the length of their processes, control the synaptic organization of the brain. The aim of this study was to investigate structural organization of microglia of the striatum and of the forebrain periventricular area in rat following transitory focal ischemia. In the absence of brain infarction, ischemic lesion was found to activate microglia, which contributed to rearrangement of striatal neuropil. As microgliocytes became activated, they changed their shape from characteristic dendritic one to oval and rounded, which are typical to amoeboid microglia. Microgliocytes were shown to be capable of proliferation.

The aim of the present investigation was to determine the neuronal population of rat telencephalon that was most sensitive to ischemic damage under the experimental condition of transient focal cerebral ischemia. It was found that 30-minute ischemia of the left hemisphere resulted in a significant decrease of neuronal population in the dorsomedial part of caudatoputamen. Local neural cell death was accompanied by a moderate activation of the astrocytes.

Hyperbaric oxygen (HBO2) causes CO2 retention in the brain that leads to the increase in cerebral blood flow (CBF) by poorly understood mechanisms. We have tested the hypothesis that NO is implicated in CBF-responses to hypercapnia under hyperoxic conditions. Alert rats were exposed to HBO2 at 5 ata and blood flow in the striatum measured by H2 clearance every 10 min. Acetazolamide, the inhibitor of carbonic anhydrase, was used to increase brain PCO2. CBF responses to acetazolamide administration (30 mg/kg, i.p.) were assessed in rats breathing air at 1 ata or oxygen at 5 ata with and without NOS inhibition (L-NAME, 30 mg/kg, i.p.). In rats breathing air, acetazolamide increased CBF by 34 +/- 7.4% over 30 min and by 28 +/- 12% over 3 hours while NOS inhibition with L-NAME attenuated acetazolamide-induced cerebral vasodilatation. HBO2 at 5 ata reduced CBF during the first 30 min hyperoxia, after that CBF increased by 55 +/- 19% above pre-exposure levels. In acetazolamide-treated animals, no HBO, induced vasoconstricton was observed and striatal blood flow increased by 53 +/- 18% within 10 min of hyperbaric exposure. After NOS inhibition, cerebral vasodilatation in response to acetazolamide during HBO2 exposure was significantly attenuated. The study demonstrates that NO is implicated in acetazolamide (CO2)-induced cerebral hyperemia under hyperbaric oxygen exposure.

The goal of work was to reveal changes in microcirculation of the rat brain and the role of nitric oxide (NO) in development of seizures at hyperbaric oxygen exposure. The Wistar rats with implanted paired platinum electrodes in left and right striatum were used for experiments. The latency of seizures was defined by the EEG, the cerebral blood flow (CBF) was measured by hydrogen clearance. One group of animals was exposed to a 5-ata oxygen, while the others before oxygen treatment were injected with: Nw-nitro-L-arginine methyl ester (L-NAME), blockator of constitutive NO synthase; 7-nitroindozol (7NI), specific inhibitor of neural NO synthase. The latency of seizures was 41 +/- 1.9 min at 5 ata oxygen exposure. CBF was decreased to 10-14% but before seizures it increased to 23 +/- 9%. L-NAME and 7NI prevented development of hyperoxygen hyperemia and onset of seizures. The results indicate occurrence of hyperbaric oxygen changes of the CBF that modulate neurotoxic effects of NO in neurons as well as in cerebral vessels.

Pathological conditions of the cerebral vessels and main arteries of the head on the side opposite to the side of the involved limbs are the etiological factors in one third of the patients. Cerebral angiography and computer tomography make it possible to verify vascular lesions of the subcortical structures which could cause the development of hemihyperkinesis . These foci of affection were most frequently located in the striapallidal system of the hemisphere contralateral to the affected limbs.

Electron microscope study of capillaries, arterioles, and venules of the cerebral cortex, strio--pallidar and nonneurosecretory complexes of hypothalamus of the man, cat, and rat revealed some details of the structure of the basal membrane and its interrelationship with adjacent astrocyte processes. Specific tight--junction type was present constantly among the adjacent membranes of glial cells. The system of the specializations and basal membrane seems to exert regulatory influence upon functioning of the blood--brain barrier.

The nature and degree of motor disorders, the degree and rate of recovery were shown to be more dependent on the localization than on the size of the cerebral infarction specified by computer-aided tomography of the drain. Localization of infarct in the posterior femur of the internal capsule proved the least favourable with regard to the recovery of motor functions.

To determine the possible role of age in motor rehabilitation, the authors compared the degree of restoration of impaired motor functions in patients of different age groups with infarction foci in the large hemispheres of the brain. Localization and size of post-ischemic changes in the cerebral substance were assessed by computer-aided tomography. By the end of the late rehabilitative period. (12 months after the development of infarction), there were no statistically significant differences between the degree of recovery of impaired motor possibilities. Most important for recovery seems to be an intactness of functionally significant structures, especially of the posterior femur of the internal capsule.