Carnosine, a specific constituent of excitable tissues of vertebrates, exhibits a significant antioxidant protecting effect on the brain damaged by ischemic-reperfusion injury when it was administered to the animals before ischemic episode. In this study, the therapeutic effect of carnosine was estimated on animals when this drug was administered intraperitoneally (100 mg/kg body weight) after ischemic episode induced by experimental global brain ischemia. Treatment of the animals with carnosine after ischemic episode under long-term (7-14 days) reperfusion demonstrated its pronounced protective effect on neurological symptoms and animal mortality. Carnosine also prevented higher lipid peroxidation of brain membrane structures and increased a resistance of neuronal membranes to the in vitro induced oxidation. Measurements of malonyl dialdehyde (MDA) in brain homogenates showed its increase in the after brain stroke animals and decreased MDA level in the after brain stroke animals treated with carnosine. We concluded that carnosine compensates deficit in antioxidant defense system of brain damaged by ischemic injury. The data presented demonstrate that carnosine is effective in protecting the brain in the post-ischemic period.

Maghemite (gamma-Fe2O3) nanoparticles were obtained by the coprecipitation of Fe(II) and Fe (III) salts with ammonium hydroxide followed by oxidation with sodium hypochlorite. Solution radical polymerization of N,N-dimethylacrylamide(DMAAm) in the presence of maghemite nanoparticles yielded poly(N,N-dimethylacrylamide)(PDMAAm)-coated maghemite nanoparticles. The presence of PDMAAm on the maghemite particle surface was confirmed by elemental analysis and ATR FTIR spectroscopy. Other methods of nanoparticle characterization involved scanning and transmission electron microscopy, atomic adsorption spectroscopy (AAS), and dynamic light scattering (DLS). The conversion of DMAAm during polymerization and the molecular weight of PDMAAmbound to maghemite were determined by using gas and size-exclusion chromatography, respectively. The effect of ionic 4,4'-azobis(4-cyanovaleric acid) (ACVA) initiator on nanoparticle morphology was elucidated. The nanoparticles exhibited long-term colloidal stability in water or physiological buffer. Rat and human bone marrow mesenchymal stem cells (MSCs) were labeled with uncoated and PDMAAm-coated maghemite nanoparticles and with Endorem as a control. Uptake of the nanoparticles was evaluated by Prussian Blue staining, transmission electron microscopy, T(2)-MR relaxometry, and iron content analysis. Significant differences in labeling efficiency were found for human and rat cells. PDMAAm-modified nanoparticles demonstrated a higher efficiency of intracellular uptake into human cells in comparison with that of dextran-modified (Endorem) and unmodified nanoparticles. In gelatin, even a small number of labeled cells changed the contrast in MR images. PDMAAmcoatednanoparticles provided the highest T(2) relaxivity of all the investigated particles. In vivo MR imaging ofPDMAAm-modified iron oxide-labeled rMSCs implanted in a rat brain confirmed their better resolution compared with Endorem-labeled cells.

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Anesthetics can either promote or inhibit the development of neurogenic pulmonary edema (NPE) after central nervous system (CNS) injury. The influence of isoflurane was examined in male Wistar rats using 1.5%, 2%, 2.5%, 3%, 4%, or 5% isoflurane in air. Epidural balloon compression of the thoracic spinal cord was performed. The development of NPE was examined in vivo and on histologic sections of lung tissue. Animals anesthetized with 1.5% or 3% isoflurane were behaviorally monitored using the BBB and plantar tests for 7 weeks post-injury. The spinal cord was examined using MRI and morphometry of the spared white and gray matter. All animals from the 1.5% and 2% groups developed NPE. Almost 42% of the animals in the 1.5% group died of severe pulmonary hemorrhage and suffocation; x-rays, the pulmonary index, and the histological picture revealed a massive NPE. More than 71% of the animals from the 2.5% and 3% groups did not develop any signs of NPE. Blood pressure after spinal cord compression rose more in the 1.5% group than in the 3% one. In the 1.5% group, the sympathetic ganglionic blockade prevented the neurogenic pulmonary edema development. Animals from the 3% group recovered behaviorally more rapidly than did the animals from the 1.5% group; morphometry and MRI of the lesions showed no differences. Thus, low levels of isoflurane anesthesia promote NPE in rats with a compressed spinal cord and significantly complicates their recovery. The optimal concentration of anesthesia for performing a spinal cord compression lesion is 2.5-3% isoflurane in air.

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