Single application of glycine in a final dose of 40 mg/kg to the surface of the parietal area of rat brain produced a potent vasodilatory effect. The diameter of arterioles increased to 250% from the baseline level 1-3 min after treatment. These changes persisted for 5-10 min. In the follow-up period the diameter of vessels progressively decreased to the baseline level. Repeated application of glycine in the same dose also induced dilation of arterioles. Application of physiological saline under similar conditions did not produce these changes.

Nitric oxide (NO) is one of the most important signal compounds in a living cell. As a typical free radical it has both toxic and physiological effects and their balance is determined by a spatial distribution of NO concentration. Moreover, some biological functions, especially NO-mediated relaxation of blood vessels, have to be time-limited. In order to circumscribe this phenomenon non steady-state mathematical model has been used for description of nitric oxide diffusion in vascular smooth muscle. It was shown that the microvascular relaxation could be observed even after a short time of NO production in the endothelium. This time is up to 3 times below that needed to reach the steady-state spatial NO gradient. However, the effect of nitric oxide essentially depends on the rate of NO production and blood vessel diameter. Furthermore, non steady-state nitric oxide concentration gradient was represented as an analytical function of time and coordinate. It is essential that this function describes a common case of one-dimensional diffusion of uncharged low-mass molecules. Thus, the results can be used for calculation of an upper estimation of experimental data.

Slow destructive processes in brain cortex were studied under deep hypoxia (anoxia). Study of the character and dynamics of DNA destruction showed that apoptosis and necrosis run in parallel under the experimental conditions. These processes typically develop in tens of hours. A similar conclusion was reached from electron microscopic study of the tissue ultrastructure. More detailed study revealed that a relatively rare type of apoptosis not involving cytochrome c release from the intermembrane space of mitochondria and not associated with opening of the mitochondrial nonspecific pore occurs under the experimental conditions. As this is occurring, the process can be slowed by high concentrations of glycine, an inhibitory neurotransmitter. The study of DNA destruction demonstrated that high concentrations of glycine selectively slow apoptosis but have almost no effect on necrosis. Glycine also drastically decreases changes in the tissue ultrastructure, particularly of mitochondria, arising under anoxia. Glycine does not notably influence the mitochondrial oxidative phosphorylation system. Study of impairment of mitochondrial function demonstrated that the oxidative phosphorylation system is not disturbed for 1 h, which is several times longer than the inhibition time of brain function under deep hypoxia. The mitochondrial respiratory system is preserved for a relatively long time (24 h). Malate oxidase activity is deactivated after 48 h. The succinate oxidase fragment of the mitochondrial respiratory chain proved especially resistant; it retains activity under anoxia for more than 72 h. A possible mechanism of the effect of high glycine concentrations is discussed.