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We analyzed changes in activity of SDH, one of the most important enzymes of the Krebs cycle, in the cytoplasm of hippocampal and cortical neurons of Mongolian gerbils (Meriones unguiculatus) at the early and delayed reperfusion period after global brain ischemia. The data indicate that SDH activity in pyramidal neurons of various hippocampal areas and in neurons of II, III and V layers of cerebral cortex after 7-min forebrain ischemia depends on both the localization of these neurons and duration of the postischemic reperfusion. SDH activity in neurons significantly increased on days 2 and 7 after reperfusion.

A new rat model of global cerebral ischemia-reperfusion was proposed via reversible occlusion of the major vessels originating from the aortic arch and supplying the brain. This technique can be used for the search and study of exogenous (pharmacological) and endogenous methods of brain protection from ischemia-reperfusion injury.

Using the method of peroxidative luminol-dependent chemiluminescence we showed that combined treatment with aspirin in low dose and dipyridamole corrects imbalance in oxidative homeostasis in mouse serum. This state resulted from a sharp increase in prooxidant processes after platelet disaggregation with normal dose of aspirin or dose-dependent inhibition of free radical processes with dipyridamole.

The choice of stromal differentiation by polypotent stem cells was studied by morphological and chemiluminescent methods. The differentiation pathway is selected on day 7 after heterotopic bone marrow transplantation and injection of estrone. The imbalance in plasma oxidant homeostasis in mice on day 7 after estrone injection is associated with drastic intensification of free-radical oxidation and blockade of antioxidant activity.

The choice of hemopoietic differentiation by polypotent bone marrow stem cells was studied by morphological and chemiluminescent methods. This choice occurred on day 7 after heterotopic bone marrow transplantation and dipyridamole administration, under the effect of oxidative homeostasis imbalance in the plasma. Dipyridamole increased total antioxidant activity and 10-fold reduced the intensity of free radical oxidation. Disaggregation therapy with dipyridamole reduced platelet count in the peripheral blood and decreased total plasma antioxidant activity.

Activation of free radical oxidation and inhibition of antioxidant activity in mouse myocardium after long-term dipyridamole treatment were demonstrated using chemiluminescent techniques. At the same time, dipyridamole 10-fold inhibited free radical oxidation and slightly increased antioxidant activity in the plasma. Dipyridamole-induced platelet disaggregation was accompanied by an increase in platelet count.