The effects of a non-selective blocker of NO synthases LNNA in a dose of 25 mg/kg and nitrates KNO3, NaNO3, Mg(NO3)(2), and Ca(NO3)(2) in doses of 5 and 50 mg/kg were studied on the model of experimental ischemic stroke induced by bilateral occlusion of the common carotid arteries. Wistar rats were randomized into 40 treatment (n=960) and 8 control (n=192) groups. Treatment group rats received injection of either nitrate, or LNNA, or a combination LNNA+nitrate. All substances were administered intraperitoneally 1 h prior to brain ischemia or 5 sec after occlusion of the common carotid arteries. Control rats received the same volume of 0.9% NaCl at the same terms. The non-selective inhibitor of NO synthases LNNA administered against the background of brain ischemia increased neurological deficit and animal mortality. Nitrate/nitrite reductase system had protective properties depending on the cation of nitrate and concentration of a nitrate during inhibition of NO synthase system under conditions of brain ischemia and hypoxia.

We studied the effect of sodium nitrite in doses of 5 and 50 mg/kg and NO synthase inhibitor L-NNA in a dose of 20 mg/kg on the course of experimental ischemic stroke caused by occlusion of both carotid arteries. Sodium nitrite and NO synthase inhibitor were administered 1 h prior to occlusion of еру carotid arteries and 5 sec after brain ischemia. Sodium nitrite in a dose of 5 mg/kg had a protective effect on the time course of neurological disorders and reduced animal mortality. NO synthase inhibitor L-NNA aggravated the neurological symptoms.

Исследовано участие оксида азота (NO) в механизмах протекторного действия при адаптации крыс линии Крушинского–Молодкиной к умеренной гипоксии, соответствующей высоте 5000 м над уровнем моря. Установлено, что селективные ингибиторы нейрональной и индуцибельной NO-синтаз (7-нитроиндазол и аминогуанидин) значительно усиливают защитный эффект кратковременной адаптации к гипоксии при развитии стрессорных повреждений у крыс этой линии.

We studied the protective role of nitric oxide (NO) in the adaptation of Krushinsky-Molodkina rats to moderate hypoxia corresponding to 5000 m altitude above sea level. Selective inhibitors of neuronal and inducible NO-synthases (7-nitroindasol and aminoguanidine) have been found to increase significantly the effect of short-term adaptation to hypoxia during the development of stress-induced damage in these rats.

OBJECTIVE:To reveal a protective role of the nitrite/nitrate reductase system in NO- synthase (NOS) inhibition in ischemic stroke.MATERIAL AND METHODS:An effect of the non-selective NOS inhibitor Nω-nitro-L-arginine (L-NNA) introduced in dose of 25 mg/kg and nitrates (КNO3, NaNO3, Mg(NO3)2, Ca(NO3) in doses of 5 mg/kg) on ischemic stroke induced by the occlusion of carotid arteries in an experimental model was studied. The animals (Wistar rats) were stratified into 20 experimental groups (n=480) and 4 control groups (n=96). One of nitrates or L-NNA along with one of nitrates or L-NNA alone were administered to experimental groups 1h before brain ischemia or 5s after carotid artery occlusion. 0.9% NaCl was used in the control rats.RESULTS:L-NNA increases neurological deficit and lethality in brain ischemia. Depending on a cation, the nitrite/nitrate reductase system may play a protective role in the inhibition of NOS-system in brain ischemia.CONCLUSION:In brain ischemia and NOS inhibition, Mg(NO3)2 has the greatest protective effect.

We found that selective inhibitors of neuronal and inducible NOS (7-nitroindazole and aminoguanidine) significantly enhance the protective effect of short-term adaptation to hypoxia on the development of stress lesions in rats Krushinsky-Molodkina.

The NO-synthase inhibitor LNNA (2,5 mg/100 g) abolished the protective effects of short-term adaptation to hypoxia (1 hour, 5000 m above sea level) on the development of stress-induced disorders on the model of acoustic stress in the Krushinsky—Molodkina rats genetically predisposed to audiogenic seizures. Using electronic spine resonance method (ESR) we also demonstrated an increase in NO production during short-term hypoxia in the blood and spleen. The results suggest that NO plays a positive role in protective effects of short-term adaptation to hypoxia.

The study examined effects of inorganic magnesium agents: magnesium nitrate Mg(NO3)2, magnesium sulfate MgSO4, and magnesium chloride MgCl2 on the development of neurological disorders and mortality in rats resulting from cerebral ischemia provoked by a single-stage bilateral occlusion of the common carotid arteries. The rats were injected with one of examined magnesium preparations (5 mg/1 kg body weight) 1 h prior to or 1-2 sec after occlusion. The control group rats were treated with physiological saline at the same terms. Irrespective of the moment of injection, magnesium nitrate demonstrated significant protective effect on dynamics of neurological disorders and mortality, while similar effects of magnesium sulfate and magnesium chloride were insignificant.

Objectives. To explore the effect of inorganic forms of magnesium (magnesium nitrate, magnesium sulfate, magnesium chloride) on the course of experimental ischemic stroke (II). Material and methods. The experimental ischemic stroke caused by the occlusion of two carotid arteries in Wistar rats was studied. Animals were divided into 6 case (n=168) and 2 control groups (n=56). In case groups, magnesium was injected 1h before the occlusion of both carotid arteries and 1-2h after the brain ischemia. Control groups received physiological solution in the same periods. Results. Magnesium nitrate, regardless of the period of injection, had the significant positive effect on the dynamics of neurological lesions and mortality of animals. Conclusions. Magnesium nitrate meets the majority of criteria required for ideal pharmacological drugs: it is inexpensive, easy available, easy injectable and does not cause any serious adverse effects.

Effects of magnesium nitrate (Mg(NO3)2) on the dynamics of neurological disorders and the lethality rate after brain ischemia induced by simultaneous bilateral occlusion of common carotid arteries were investigated in rats. Mg(NO3)2 administered in doses of 5 mg/1000 g and 50 mg/1000 g 60 min before and 1–2 s after the occlusion of both common carotid arteries statistically reduced the severity of neurological impairment and the death rate of rats.

Objectives. To study the effect of inhibitors of neuronal and inducible NO-synthase on the development of hemorrhagic stroke in rats Krushinsky-Molodkina (KM) without adaptation to hypoxia and with short-term adaptation to hypobaric hypoxia. Material and methods. Ninety rats were included in the study. Experiments with short-term adaptation to hypobaric hypoxia were performed on 48 rats. The inhibitor of inducible NO-synthase (aminoguanidine, "Sigma") or the inhibitor of neuronal NO-synthase (7-nitroindasol, "Sigma") were injected in dosage 2.5 mg/100g intraperitoneally. Results. Selective inhibitors of neuronal and inducible NO-synthase had a protective effect on stress injuries in KM rats. The inhibitor of neuronal NO-synthase was more effective than the inhibitor of inducible NO-synthase in the experiments without adaptation to hypoxia. Markedly greater protective effect was achieved by the simultaneous introduction of inhibitors of neuronal and inducible NO-synthase. The greatest protective effect in the development of stress damage in rats of KM was observed in short-term adaptation to hypobaric hypoxia with simultaneous introduction of both inhibitors. Conclusions. It can be assumed that an excessive amount of NO produced by neuronal and inducible NO-synthases during the acoustic exposure in KM rats leads to stress damage. Use of selective inhibitors reduce the excess NO synthesis and the development of audiogenic stress damage caused by hemorrhagic stroke.

Effect of potassium nitrate (KNO 3 ) on the dynamics of neurological disorders and lethality in rats as sequelae of brain ischemia induced by a single-step bilateral common carotid artery occlusion were investigated in Wistar rats. KNO 3 at a dose of 5 mg/1000 g administered 60 min prior to the occlusion of the two carotid arteries reliably reduced the severity of neurological disorders and lethality in rats.

Experiments were performed on the model of ischemic stroke due to bilateral occlusion of the carotid arteries. Nitrates had various effects on the dynamics of neurological disorders and mortality rate of Wistar rats, which depended on the cation type and concentration.

The protective effect of cortexin was investigated with the use of acoustic stress hemorrhagic stroke model. A significant decrease of 8-oxo-2'-deoxyguanosine to 2'-deoxyguanosine ratio in the DNA molecule was shown using brain slices of cortexin treated Krushinsky-Molodkina rats.

The protective effect of cortexin was investigated with the use of acoustic stress hemorrhagic stroke model. A significant decrease of 8-oxo-2'-deoxyguanosine to 2'-deoxyguanosine ratio in the DNA molecule was shown using brain slices of cortexin treated Krushinsky-Molodkina rats.

Effects of nitrates NaNO(3), KNO(3), Mg(NO(3)) 2 on animals (Wistar rats) were studied on the basis of the experimental model of ischemic stroke induced by the occlusion of two carotid arteries. The animals were divided into two groups: the main group (n=60) and the control group (n=30). Three series of experiments were conducted. In each experiment, the rats of the main group were treated with one of nitrates and the control group was treated with physiological solution. It has been shown that nitrates exert either positive or negative effect depending on the cation type, nitrate concentration and the duration of their action on the dynamics of neurologic disturbances. Conditions of the development of neuroprotective effect of nitrates are discussed.

We studied the effect of locomotor activity on the ultrastructure of cerebellar neurons, neurological disturbances, and survival rate in Krushinsky–Molodkina rats during the development of hemorrhagic induced by acoustic stress. In animals with high spontaneous locomotor activity, severe edema of cerebellar neurons (resulting in the destruction of surrounding structures) and swelling of the synapses (terminals of mossy fi bers on granule cell dendrites) were observed. By contrast, the areas of intracerebral, subdural, and subarachnoid hemorrhages were lower in rats under conditions of forced rest.