The central nervous system both anatomically and functionally has a certain autonomy in comparison with the rest of the system thanks to the so called barriers dividing brain from both blood and cerebro-spinal fluid. Capillary vessels in brain are additionally surrounded by protoplasmic process of neuroglial cells. They are astrocytes which by means of protoplasmic process hermetically surround capillary vessels from the outside. Owing to that astrocytes create an additional layer, that has to be overcome by chemical compounds circulating in blood (2). Brain barrier fulfils an immunological function. It protects brain tissue against fluctuations in concentration of respective components occurring in blood plasma and against destructive blood components (2, 7). Lowering of brain flow of blood below 10-15 ml/100 g/min causes deficit of glucose and oxygen, indispensable for proper oxido-reductive processes. The most important factor determining brain tissue damage is a constant shortage of high energetic phosphate. Damage to mechanisms depending on energy causes ischaemic depolarisation phenomenon, after which potassium ions come out of cells and sodium and calcium ions come into them. Neurotransmitters, stimulating amino acids including, are being freed in a quantity that is conductive to toxic activity. Fall of blood flow causing acidosis provokes disturbances in vessel self-regulation, and lactates created are additional factor that damages tissues. Pathophysiological changes mentioned above lead to heavy injury and death of cells (3, 12). The intensifying acidosis and the process of maturing of morphological changes in ischaemic focus cause a rise in penetrability of blood-brain barrier (1, 2, 8). Works considering behaviour of blood-brain barrier in the process of brain stroke, are for the most part based on experimental models.