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We developed a new minimally invasive model of spinal cord ischemia in rats: intravascular occlusion of the abdominal aorta and its branches. This model can be used on small laboratory animals and allows qualitatively and quantitatively evaluating the morphofunctional state of the nervous system during spinal cord ischemia by clinical manifestations and histological changes. Selective intravascular occlusion determines minimal invasiveness and adequacy of the proposed model to in vivo pathological processes. This model of spinal cord ischemia can be used in experimental pharmacology for evaluation of neuroprotective activity of various drugs and bioactive substances.

Adenosine, an agonist of A1 adenosine receptors, and hypoxic preconditioning exert a neuroprotective effect on brain cells. The blocker of A1 adenosine receptors aggravates metabolic disturbances in the brain and removes the protective effect of cyclopenyladenosine and ischemic preconditioning.

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Adenosine and its analogs N6-cyclohexyladenosine (CHA) and N-ethylcarboxamideadenosine (NECA) are highly effective when injected into the lateral ventricle in very low doses (by 1-2 orders lower than subcutaneously). The protective effect of A-agonists is considered to be mediated by a central mechanism and reahzed via A-receptors of the brain: the effects of low doses of A-agonists are mediated by At-receptors, whereas higher doses exert an extra Au-effect. Key Words: A-receptor agonists; antihypoxants; cerebral ischemiaAdenosine and other A-agonists are characterized by a higJa cerebroprotective effect (CPE) in cerebral ischemia, as has been shown in experimental occlusion of cerebral arteries, in in vitro reproduction of neuronal ischemia [8,11,13,14], and in total ischemia of the brain [3,4], in which CPE was due not to an increase in the cerebral bloodflow, but rather to protection of the neurons themselves [3]. Similar results were observed in other models [8,13]. This is in line with the data on a direct effect of A-agonists on the brain, reducing its activity [2,6,8,11,13]. However, the hypothesis on the central mechanism of A-agonist CPE is still to be directly confirmed in experiments [10].We studied A-agonist CPE for intracerebroventricular injection and compared it with that for subcutaneous injection. MATERIALS AND METHODSExperiments were carried out with 255 white mice of both sexes weighing 18-20 g, Adenosine manufactured by Reanal (Hungary), CHA synthesized in were used. The agents were injected into the right lateral cerebral ventricle in the following manner: the skin was cut from the upper part of the head and a microsyringe needle was inserted to a depth of 3 mm at a point 1-2 mm to the fight of the chiasma of the cranial; 10 txl of solution was then injected (the method was recommended by N. K. Popova and I. P. Voronova). The adequacy of the method was repeatedly confirmed by injection of stain. The duration of gasping (agonal respiration) after decapitation was an indicator of brain resistance to total ischemia [3,4]. Since gasping duration did not conform to the normal distribution [4], the resuits were analyzed using the nonparametric Wilcoxon-Mann-Whitney U test. EDs0 was assessed by probit analysis after Litchfield-Wilcoxon-Roth [1].