Hemorrhagic stroke (HS) in newborns is an important but understudied problem. HS occurs in 2 to 13 children per 100 000 per year in developed countries. The incidence of HS in low birth weight infants ( neonatal intensive care units worldwide. Bleeding generally occur during the second post-natal day, with the average being 48 hours after birth. Most infants in this critical period are asymptomatic or demonstrate subtle signs that are easily overlooked and cannot be readily detected with the most widely used neuroimaging procedure in infant. The long time it was believed that hemorrhage is the most common type of brain bleeding only in preterm newborns but in term newborns HS is relatively uncommon. But latest prospective magnetic resonance imaging studies of asymptomatic term newborns suggest that HS is much more frequent that previously thought. Important notice that advancements in neonatal hemorrhagic stroke care is hampered by the lack of understanding regarding the underlying pathophysiological mechanisms and a paucity of prospective data regarding treatment and outcomes. Currently, there are no proven strategies for the medical management of childhood stroke. Recommendations and treatment guidelines have largely been extrapolated from adult data. The lack of diagnostic markers, effective technology for early determination of risk for HS and treatment of HS in newborns explains the high rate of neonatal death and less optimistic neurologic prognosis in infants after HS. About 85% of infants with HS develop major cognitive deficit and approximately 75% of these infants need special education in school. A small number of animal studies have examined the mechanisms of ICH in neonatal period. There is no experimental method is closest to the natural origin HS. A reproducible animal model of HS mimicking the mechanisms underlying acute and delayed HS-induced brain injury is an invaluable tool for our understanding of pathophysiological processes responsible for development of HS and consequences after HS as well as for evaluating potential therapeutic interventions. We developed a new original model of HS in newborn rats using harmful effects of infrasound on the brain (The method of modeling of intracranial hemorrhage in newborn rats / Patent RF № 2052865). The results of MRI and histological analysis of the brain tissue of newborn rats showed multiple rupture of small vessels in the cortex in next day after infrasound influences. Notice, that in term neonates HS usually occurs in the subdural or subarachnoid space, i.e. superficially. Thus, our model allows non-invasively to induce superficial hemorrhages in the cortex area of brain that mimics clinical topography of brain bleeding in full term newborns. The results of DOCT and speckle imaging studies of relative cerebral blood flow (rCBF) in cortex through fontanel (dura left intact) in newborn rats show that cerebral venous is more informative platform for prognosis of risk for HS – they response first to infrasound influences by dilation (results from sagittal sinus) which is progressed gradually with time after sound stress. The relaxation of veins of cortex is accompanied by development of venous insufficiency and decrease blood outflow from the brain. This is reason secondary response of small artery and capillaries in cortex. 24h after sound stress histological data shows increasing of size and number of visible arterial vessels as well as swelling of venous and arterial blood vessels in the brain cortex. The data of oxygen saturation of brain tissue show that arterial hypotension after HS is associated with hypoxia. Using pharmacological tests and immunofluorecent and immonblot analysis of brain tissue we found that the high activation of non-innervated beta2-adrenoreceptors which stimulate ATP-sensitive K+-channels and Gs-protein-dependent activation of protein kinase A and β-arrestin-mediated signalling pathways, trigger stress-induced rupture of cerebral vessels. Also, we obtained high expression of Sur1-receptors modulating of KATP-channels in the brain of newborn rats with HS compared with healthy animals. Thus, non-innervated processes of regulation of CBF (vascular beta2-sdrenereceptors and KATP-channels) can play an important role in development of pathological changes in cerebral circulation associated with HS. Using intravenous injection of glibenclamide – specific blocker of KATP-channels and a new promising drug in treatment of stroke, we found a good therapeutic effect of glibenclamide but only in 37% of sick rats. Other rats (67%) demonstrated decrease in permeability of brain blood barrier that is a key reason for limitation of availability of glibenclamide. These findings can be useful for better understanding the symptoms and mechanisms of HS in newborns and also for the further study of sensitive markers of predictability of HS and new therapeutic approaches in infants with HS during the first days after birthday. Supported by grants №14.Z50.31.0004 and № 14-15-00128.