7 results match your criteria: "State Research Institute of General Pathology and Pathological Physiology[Affiliation]"

The development of immediate and delayed long-term resistance to hypoxia during a course of intermittent normobaric hypoxia (15 daily sessions of alternating exposure to 10% O2 and atmospheric air for 1 h) correlated with biphasic expression of HIF-1α in neocortex of hypoxia-intolerant rats, which suggests involvement of this protein factor not only in the formation of long-term adaptation, but also in triggering immediate adaptation to hypoxia. Both processes develop under conditions promoting down-regulation of oxidative modification of LDL and increasing tolerance of biological membranes to hypoxia in the absence of activation of the free radical processes, which therefore do not trigger HIF-1α expression under these conditions. Neither cytokines nor NO are the inducers of immediate adaptation, and they are not related to HIF-1α expression during the early post-hypoxic period.

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We studied the effect of Cl(-) (10-75 mM) and HCO(3)(-) ions (10-25 mM) on the ATP-dependent GABA(A) receptor-coupled Cl(-) channel (Cl(-)-ATPase) in rat brain plasma membranes. The total enzyme activity was detected in the presence of both anions at a Cl(-)/ HCO(3)(-) ratio of 5:1 (Cl(-), HCO(3)(-)-ATPase). Specific inhibitors of P-type transport ATPases (N-ethylmaleimide, o-vanadate, and oligomycin) suppressed Cl(-), HCO(3)(-)-ATPase, while the Cl(-)- and HCO(3)(-)-ATPase activities were low sensitive to these ligands.

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Application of choline (5 and 10 mM) to electrically stimulated (1 Hz) rat hippocampal slices evoked epileptoid activity manifested by generation of extra population spikes. Application of methyllycaconitine (10 nM), a specific agonist for α7-subunit of nicotinic acetylcholine receptors, did not prevent generation of extra population spikes. In contrast, pretreatment of slices with Mg(2+) (5 mM) or blockade of NMDA-type glutamate receptors with MK-801 (100 μM) prevented generation of the extra population spikes.

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In 12 patients with myasthenia, the content of β(2)-adrenoreceptors on the cell surface and activity of intracellular lymphocytic enzymes were determined by EIA and biochemical methods, respectively. In comparison with the normal, these patients demonstrated pronounced elevation in the content of β(2)-adrenoreceptors and significant changes in activity of lymphocytic enzymes. In 10 of 12 patients, administration of the agonists to β(2)-adrenoreceptors resulted in health improvement accompanied by normalization of EMG and immunobiochemical indices.

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Mechanism of adaptation of the vascular system to chronic changes in nitric oxide level in the organism.

Bull Exp Biol Med

December 2006

State Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences; Institute of Chemical Physics, Russian Academy of Sciences, Moscow, Russia.

We studied the possibility of directed modulation of the efficiency of NO storage in rats due to adaptation to the chronic changes in plasma NO level. The efficiency of NO storage increased during long-term maintenance of high plasma level of NO and decreased in NO-deficient states. The compensatory changes in NO storage capacity of vessels depending on its organism content represent a new mechanism of adaptation of the cardiovascular system to chronic excess or deficit of NO, while directed modulation of this process can be important for the protection of the organism against both surplus or shortage of NO.

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Analysis of contribution of sympathetic and parasympathetic systems into heart rate variability carried out using atenolol and atropine showed that August rats are characterized by enhanced tone of the sympathetic system and reduced tone of the parasympathetic system compared to Wistar rats. Reduced tone of the parasympathetic system is also confirmed by lower sensitivity of the baroreflex. Blockade of NO synthesis with Nw-nitro-L-arginine more markedly increased blood pressure variability in August rats compared to Wistar rats.

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Chronic administration of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (30 mg/kg) to C57BL/6 mice caused death of all animals within 7 days. Dipeptide analog of neurotensin active site injected with this neurotoxin protected the mice from death even after 2-week intoxication. When younger mice and lower dose of neurotoxin (25 mg/kg) were used, all animals survived, but after 2 weeks they developed parkinsonian syndrome with muscular rigidity, akinesia, decrease in motor and explorative activities.

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