Changes in functional and metabolic activities of the brain were evaluated by EEG and positron-emission/computer tomography with 18F-fluorodeoxyglucose in patients with neuropathic pain syndrome previous to and 3 months after implantation of a system for chronic epidural spinal cord stimulation. In most cases, the use of a nerve stimulator was followed by alleviation of neuropathic pain and partial normalization of functional and metabolic activities of brain structures responsible for pain perception, emotiogenic, behavioral, and autonomic responses.
It has been proposed to assess functional and metabolic state of the brain nervous tissue in terms of bioelectrical parameters. Simultaneous recording of the DC potential level and total slow electrical activity of the nervous tissue was performed in the object of study by nonpolarizable Ag/AgCl electrodes with a DC amplifier. The functional and metabolic state of the brain was determined in terms of enhancement or reduction in the total slow electrical activity and positive or negative shifts in the DC potential level.
The antioxidant effect of an adenosine A1 receptor agonist cyclopentyladenosine was studied on the model of focal cerebral ischemia. Ischemic injury of the brain was accompanied by changes in LPO processes (in the blood and brain tissue) and failure of some factors for antioxidant protection (peroxidase and catalase) that inactivate reactive metabolites. Changes in the ratio between LPO and antioxidant protection were less pronounced after treatment with cyclopentyladenosine.
We developed a new minimally invasive model of spinal cord ischemia in rats: intravascular occlusion of the abdominal aorta and its branches. This model can be used on small laboratory animals and allows qualitatively and quantitatively evaluating the morphofunctional state of the nervous system during spinal cord ischemia by clinical manifestations and histological changes. Selective intravascular occlusion determines minimal invasiveness and adequacy of the proposed model to in vivo pathological processes. This model of spinal cord ischemia can be used in experimental pharmacology for evaluation of neuroprotective activity of various drugs and bioactive substances.
Acute myocardial infarction (AMI) is one of the main causes of mortality among the able-bodied population in Russia and the population of economically developed countries. In recent years, deaths from AMI in the USA and Europe have not decreased. This is due to the lack of highly effective drugs for the treatment of AMI. One of the promising drugs to improve the survival of patients with AMI is erythropoietin. We searched for full-text publications in the PubMed database and on the website of the journal Nature. In studies performed on animals, it was shown that erythropoietin (5000 U/kg) is able to increase cardiac tolerance to ischemia and reperfusion due to activation of a number of kinases (PKC, ERK1/2, Akt, JAK2, PI3K) and due to GSK-3β kinase inactivation. Erythropoietin prevents post-infarction remodeling of the heart and enhances the process of myocardial neovascularization in rats and dogs. Erythropoietin in used doses (on the average 1000 U/kg) does not affect infarct size in patients with AMI and does not have an effect on post-infarction ventricular remodeling in humans. The reason for this discrepancy between experimental and clinical data remains unclear. It is possible that the use of large doses of erythropoietin or the use of its analogues that do not affect erythropoiesis can prevent the development of post-infarction cardiac remodeling in humans.
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