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Abstract Preparations of I125-labeled monoclonal antibodies against neurospecific enolase and mouse plasma IgG1 were injected intravenously to rats immediately after unilateral occlusion of the middle cerebral artery. Radioactivity of I125-labeled monoclonal antibodies against neurospecific enolase in the brain tissue progressively increased, reached a maximum by the 48th hour, and remained practically unchanged after 72 h. At the same time radioactivity of labeled IgG1 in the brain tissue and radioactivity of both preparations in the blood, liver, spleen, kidneys, heart, and lungs decreased over 72 h. Selective accumulation of I125-labeled monoclonal antibodies against neurospecific enolase was less significant in the brain tissue of the contralateral hemisphere and cerebellum not exposed to ischemia. [ABSTRACT FROM AUTHOR]

Abstract Preparations of I125-labeled monoclonal antibodies against neurospecific enolase and mouse plasma IgG1 were injected intravenously to rats immediately after unilateral occlusion of the middle cerebral artery. Radioactivity of I125-labeled monoclonal antibodies against neurospecific enolase in the brain tissue progressively increased, reached a maximum by the 48th hour, and remained practically unchanged after 72 h. At the same time radioactivity of labeled IgG1 in the brain tissue and radioactivity of both preparations in the blood, liver, spleen, kidneys, heart, and lungs decreased over 72 h. Selective accumulation of I125-labeled monoclonal antibodies against neurospecific enolase was less significant in the brain tissue of the contralateral hemisphere and cerebellum not exposed to ischemia. [ABSTRACT FROM AUTHOR]

Enzyme immunoassay of the serum neurospecific antigens (gliofibrillar acid protein and neurospecific enolase) was used for evaluation of the resistance of the blood-brain barrier in Wistar rats with perinatal hypoxia and ischemia of the CNS. Perinatal hypoxia and ischemia of the CNS was modeled by two methods: ligation of the common carotid artery in 7-day-old rats followed by 3.5-h hypoxic hypoxia or 15-min anoxic exposure of fetuses isolated via hysterectomy on day 21 of gestation. Enzyme immunoassay of serum gliofibrillar acid protein and neurospecific enolase in control an experimental rat pups was carried out once a week during 3 months. In controls serum levels of gliofibrillar acid protein and neurospecific enolase virtually did not change during postnatal development, while in animals with cerebral hypoxia and ischemia induced in fetuses by both methods serum concentration of neurospecific enolase sharply increased 1 week after the injury and increased on weeks 6 and 10. The content of gliofibrillar acid protein was maximum on week 1 and later considerably varied, the peaks of its concentrations observed on weeks 3 and 8 preceded the increase in neurospecific enolase activity in peripheral blood. [ABSTRACT FROM AUTHOR]

Seven-day-old Wistar rat pups were subjected to unilateral occlusion of the common cerebral artery and maintained in oxygen-low atmosphere. Neurological and behavioral changes were monitored for 12 weeks. The survival rate of treated animals was 90%. Body weight gain in these rats was lower than in the control. Neurological deficit was maximum 1 week after treatment and slightly regressed by the 12th week. Locomotor activity in treated rats was higher than in controls. Administration of ketamine in subanesthetic doses caused permanent ipsilateral rotational asymmetry in animals. Spatial disorientation and cognitive deficit in rats with hypoxic-ischemic damage to the central nervous system were revealed in passive avoidance, Y-maze, and rotarod tests. The total area of the hemisphere decreased, while the area of the lateral cerebral ventricle increased at the side of occlusion over the first 4-5 weeks of postnatal development. The size of the ipsilateral hemisphere remained low in adult animals. [ABSTRACT FROM AUTHOR]

Neurological, locomotor, and behavioral changes in 20 Wistar rats with permanent proximal occlusion of the middle cerebral artery and 18 control sham-operated animals were monitored for 2 months at 10-day intervals. Neurological deficit was maximum immediately after occlusion (3.0±0.6 points), then progressively decreased, but did not completely disappear (0.70±0.06 points on day 60). In control animals neurological status returned to normal on days 10-15. The degree of ketamine-induced rotational asymmetry was 4.0±0.7 rpm over 40 days after surgery and decreased to 2.5±0.6 rpm on day 60. In control rats this parameter only transiently increased to 1.00±0.03 rpm (tδ=2.5, p<0.05). The time of stay on a rotarod and the latency of passive avoidance in rats with focal cerebral ischemia were lower than in control animals throughout the experiment. The results of complex tests can be used in the experimental search for new drugs for the therapy and rehabilitation of stroke patients. [ABSTRACT FROM AUTHOR]

Intraperitoneal injection of ketamine in subanesthetic doses to Wistar rats with unilateral occlusion of the middle cerebral artery caused ipsilateral rotation (2-10 rpm), which was recorded in an automatic rotameter. The optimal dose of ketamine was 50 mg/kg. The animals were examined in an automatic rotameter for 40 min. Motor asymmetry persisted for no less than 2 months after surgery. According to the neurological test (Menzies scale) motor asymmetry in animals with focal brain ischemia persisted for no more than 30 days. The degree of ketamine-induced motor asymmetry in intact rats was 0.10±0.03 rpm. [ABSTRACT FROM AUTHOR]