Expression of Nestin and Glial Fibrillary Acidic Protein in the Marginal Ischemic Zone of the Brain in SHR Rats.

We studied spatial organization and structural characteristics of striatal glial cells in spontaneously hypertensive rats (SHR) in 48 h after 30-min focal ischemia. Immunocytochemical analysis of nestin and glial fibrillar acidic protein (GFAP) revealed 3 types of activated astrocytes: expressing only nestin, only GFAP, or both markers. There were no nestin-immunopositive astrocytes in the striatum of sham-operated rats. In cells expressing nestin and GFAP, localization of these markers did not completely coincide, which can be explained by different functions of these proteins or formation of heterodimers of nestin with other intermediate filament proteins.

Experimental model of osteonecrosis of the jaw in rats treated with zoledronic acid.

We have examined the development of medication-related osteonecrosis of the jaws (MRONJ) in rats with no previous accumulation of zoledronic acid in the mandible. Ten male Wistar rats (weight 350-400g) were anaesthetised with chloral hydrate 450mg/kg intraperitoneally and the first and second mandibular molars on the left side were extracted. The five experimental rats were given six injections of zoledronic acid 0.18mg/kg over the next four weeks (total dose 1.08mg/kg). Two injections were given at once as an intravenous bolus injection (0.36mg/kg). Then rats were given 4 injections (0.18mg/kg) with 1 week interval over the next four weeks, after which they observed for a further four weeks. The five control rats were injected with saline. At the end of the eighth week, the animals were killed by asphyxiation in a carbon dioxide chamber, and their bone structure was visualised using cone-beam computed tomography (CT) and Galaxis software. We then studied the mandibles histopathologically to investigate the incidence of necrosis and infiltration of inflammatory cells. The cone-beam CT images in the experimental group showed deficiencies in the bone structure in the extracted molar area of the lower alveolar ridge. The histological findings in the mandibles of the group given zoledronic acid showed necrosis and infiltration of inflammatory cells, which were not present in the control group. We conclude that the immediate effect of zoledronic acid on the bone tissue during regeneration is an important factor in the development of MRONJ, in addition to the previously reported effects of the duration of treatment with zoledronic acid.

[Preconditioning by physical factors: role of active forms of oxygen].

In the review mechanisms of protective action of a hyperthermia, light and low-intensity ultrasonic radiation are considered. These physical factors don't cause oxygen starvation, however promote the increase of organ's tolerance to an ischemia/hypoxia. On materials of original articles the analysis of preconditioning mechanisms cause by high temperatures, low-intensive ultrasonic and laser irradiation was carried out at ischemia. By comparison of processes in tissues at influence by physical factors the general triggers--active forms of oxygen (O2*, H2O2, HO*) were revealed.

[Creatine in a metabolism of cell and its protective action at brain ischemia].

The aim of this review was the discussion of creatine involvement in metabolism of nervous tissue cells. The questions of creatine penetration through the blood brain barrier and creatine transporter expression were raised. Also mechanisms of creatine protective effect were considered at experimental models of brain ischemia. It was shown that creatine was involved in energy metabolism (creatine phosphate synthesis), inhibition of excitotoxicity. Besides it had antioxidant and antiproliferative effects. The creatine delivery problem was also discussed. Synthesis of substances capable to get through the blood brain barrier without CRT was the possible solution of the problem. The most perspective substances were creatine amides apparently capable to move through cell membranes without amino acid transporters. Prospects of their application were discussed.

[Cytoprotective effect of creamide drug in the experimental model of the brain ischemia/reperfusion in rats].

The influence of creatine or its derivates on the cell energy potential may be one of the possibl approaches to induce neuroprotection. Effect of creamide (creatinylglycine ethylic ether fumarate) on the brain injury was studied in the experimental model of the brain ischemia/reperfusion in rats. The experiments were carried out in 14-20 weeks old male Wistar rats weighing 240-300 g, anesthetized by chloral hydrate (430 mg/kg). Creamide was administered intravenously at the doses of 50, 70, 140, and 280 mg/kg. For comparison phosphocreatine was used at the dose of 255 mg/kg. Creamide and phosphocreatine were administered intravenously (in volume of 1 ml within 5 min) 30 min before cerebral middle artery occlusion. Focal cerebral ischemia for 30 min was produced by endovascular suture occlusion with the subsequent 48 h reperfusion period. Creamide administration resulted in dose-dependent decrease of brain ischemic injury. Creamide administered at the doses of 140 and 280 mg/kg was more effective as compared with phosphocreatine (255 mg/kg). The data obtained open new perspectives for further research and development of new creatine-derived drugs with neuroprotective action.

[Effect of intragastric creatine glycine ethylic ether fumarate administration in a rat model of occlusive ischemia].

The aim of the study was to investigate neuroprotective effect of creatine glycine ethylic ether fumarate (creamide). The methods involved intragastric administration of creamide in doses of 30 and 50 mg/kg twice a day for 10 days. Focal 30 minutes cerebral ischemia model by endovascular suture occlusion of the middle cerebral artery in a rat with subsequent reperfusion period for 48 hours was produced. Assessment of creamide stability in gastric juice was performed. Ischemic lesion volume accompanying focal ischemia was visualized and determined. Similar infarction patterns had been found with histological methods. Garcia scale was used for clinical study of neurological deficit in rats. Our data suggest a significant neuroprotective effect of creamide in dosage 50 mg/kg administered twice a day which decreased brain lesion volume produced by ischemic and reperfusion injury.

Effects of helium-neon laser irradiation and local anesthetics on potassium channels in pond snail neurons.

Intracellular dialysis and membrane voltage clamping were used to show that He-Ne laser irradiation of a pond snail neuron at a dose of 0.7 x 10(-4) J (power density 1.5 x 10(2) W/m2) increases the amplitude of the potential-dependent slow potassium current, while a dose of 0.7 x 10(-3) J decreases this current. Bupivacaine suppresses the potassium current. Combined application of laser irradiation at a dose of 0.7 x 10(-3) J increased the blocking effect of 10 microM bupivacaine on the slow potassium current, while an irradiation dose of 0.7 x 10(-4) J weakened the effect of bupivacaine.

[Influence of He-Ne laser irradiation and local anesthetics on potassium channels in the snail neurons]. / Deistvie gelii-neonovogo lazernogo izlucheniia na kalievye kanaly neironov prudovika.

Using clamp method it had been shown that He-Ne laser irradiation of the snail neurons increases the amplitude of voltage-gated slow potassium currents in dose of 0.7 x 10(-4) (fluence 1.5 x 10(2) Wt/m2) and decreases it in dose 0.7 x 10(-3). Bupivacaine and lidocaine suppressed potassium currents. Laser irradiation in dose 0.7 x 10(-3) enhanced the inhibitory effect of bupivacaine (10 mcM) and in dose 0.7 x 10(-4) it decreased the inhibitory effect of bupivacaine. The results of the study suggest mechanisms of the He-Ne laser irradiation effect in combination with pharmacological substances on ion channels of electrically excitable cells.

[Effect of the He-Ne laser irradiation on resistance of the isolated heart to the ischemic and reperfusion injury]. / Vliianie izlucheniia He-Ne lazera na ustoichivost' izolirovannogo serdtsa k ishemicheskomu i reperfuzionnomu povrezhdeniiu.

The aim of this work was to investigate the myocardial protection against ischemia/reperfusion using low level laser irradiation (LLLI). It has been shown that pulse pressure was higher in the period of post-ischemic reperfusion as compared with the control group. It provided a better restoration of myocardial contractility as well as increasing of coronary flow in the reperfusion period. The amount of ventricular rhythm disorder episodes decreased. These effects of laser application were registered in conditions of coronary flow reduction less than 50%. One of the suggested mechanisms of laser effect is an ATP-sensitive channel activation.