Uvod: Kod velikog broja pacijenata nakon ishemijskog moždanog udara (IMU) dolazi do razvoja kognitivnih poremećaja, naročito u domenima pažnje, radne memorije i
 izvršnih funkcija, koji značajno utiču na kvalitet života i funkcionalnu nezavisnost. Iako se u kliničkoj praksi za procenu kognitivnih disfunkcija najčešće koriste
 standardizovani neuropsihološki testovi, raste potreba za objektivnim neurofiziološkim markerima koji mogu precizno reflektovati stepen oštećenja i pomoći u predikciji
 oporavka kognitivnih funkcija. Jedan od najperspektivnijih kandidata je kognitivno evocirani potencijal P300, pozitivan talas dugih latencija koji se javlja približno 300
 milisekundi nakon prezentacije značajnog (ciljnog) stimulusa, i smatra se neuralnim korelatom pažnje, selektivne obrade informacija i radne memorije.
 Cilj rada je ispitivanje značaja kognitivno evociranog potencijala P300 u identifikaciji i praćenju kognitivnih disfunkcija nakon IMU
 Metode rada: Studija je sprovedena kao prospektivno istraživanje u koje je uključeno 60 pacijenata sa prvim klinički verifikovanim ishemijskim moždanim udarom (29
 muškaraca i 31 žena, starosti od 44 -75 godina) i 30 zdravih ispitanika u kontrolnoj grupi (16 žena i 14 muškaraca, starosti 45-68 godina). Bioelektrična aktivnost mozga
 registrovana je pomoću srebro-hlorid elektroda koje su postavljane na centralnoj liniji skalpa, frontalno (Fz), centralno (Cz) i parijetalno (Pz) prema standardnom “10-20
 međunarodnom sistemu.” Za dobijanje P300 KEP korištena je “oddball” paradigma sa 80% neciljnih i 20% ciljnih stimulusa. Procena kognitivnog i afektivnog statusa
 sprovedena je primenom neuropsihološke testne baterije koja je uključivala: Mala skala za procenu mentalnog statusa (MMSE), Test praćenja traga  forma A i B, Revidirana
 Vekslerova skala pamćenja (subtestove mentalne kontrole, verbalnog i vizuelnog raspona), Spielbergerov test anksioznosti i Bekova skala depresivnosti (BDI). Funkcionalni
 status bolesnika procenjivan je Barthel indeksom (BI). Registracija P300 i neuropsihološka testiranja obavljena su u akutnoj fazi bolesti i tri meseca nakon moždanog udara.
 Rezultati: Latencije P300 talasa kod pacijenata sa moždanim udarom bile su značajno duže u poređenju sa kontrolnom grupom nad svim posmatranim arealima mozga (Fz, Cz,
 Pz p<0,001), a amplitude P300 su bile značajno manje kod obolelih samo na Pz elektrodi (p= 0,02). Uočena je tendencija oporavka: latencije su bile statistički značajno kraće
 tri meseca nakon prve registracije (Fz p=0,02, Cz p<0,01, Pz p<0,01). Nasuprot tome, amplitude P300 potencijala se nisu značajno promenile tokom praćenog perioda.
 Zabeležena je negativna korelacija između latencije P300 i Barthel indeksa u akutnoj fazi (Fz r = -0,58, Cz r = -0,36, Pz r = -0,45; sve p<0,01), kao i tri meseca nakon udara
 (Fz r = -0,54 p=0,015, Cz r = -0,42 p<0,01, Pz r = -0,54 p<0,01). Takođe je pronađena statistički značajna korelacija između latencije P300 i rezultata na neuropsihološkim
 testovima pažnje i izvršnih funkcija.
 Zaključak: Dijagnostički značaj P300 ogleda se u njegovoj sposobnosti da detektuje blage i subkliničke kognitivne deficite koji često ostaju neprimećeni standardnim
 neuropsihološkim testovima. Promene u parametrima P300 u ranoj fazi mogu imati prognostički značaj u predviđanju funkcionalnog oporavka pacijenata nakon IMU.  Rezultati
 ovog istraživanja podržavaju uvođenje P300 kao komplementarne metode u proceni i longitudinalnom praćenju kognitivnih disfunkcija nakon IMU.  U budućnosti, integracija
 P300 sa neuroimaging metodama i neuropsihološkim testovima mogla bi doprineti ranijem prepoznavanju pacijenata sa povećanim rizikom od trajnih kognitivnih oštećenja.
 Ključne reči: P300, ishemijski moždani udar, potencijali izazvani događajem

Oxidative stress plays an important role in development of ulcer lessions of the rats exposed to indomethacin induced stress. It has been suggested that endogenous opioids releassed during the stress may attenuate gastric ulcer lesions. The aim of this study was to investigate effects of morpine on development of ulcer lessions, pathohistological alterations and antioxidative status in stomach of the rats exposed to indomethacin induced stress. Research was performed on adult, male Wistar rats weighting 200-230 g. Indomethacin stress was induced by intragastric administration of indomethacin at a dose of 20 mg/kg b.w. 6 hours before sacrificing. Morphine was applied intraperitoneally, in the doses of 10 mg/kg b.w. 15 minutes before indomethacin induced stress. The size of lesions in the form of petechiae and erosion, is expressed as the total surface of changes (mm2), i.e. ulcer index (UI). The pathohistological samples were analyzed by Leica DML S2 light microscope, and specific changes were photodocumented with Canon Power Shot S70 digital camera. In the homogenate of the stomach, the activity of catalase (CAT), glutathione peroxidase (GSHPx), glutathione reductase (GR) and xanthine oxidase (XOD) were measured, as well as the reduced glutathione content (GSH) and the lipid peroxidation intensity (Lpx). Morphine significantly reduced the ulcer index (UI) in animals exposed to indomethacin stress and the presence of large amounts of mucus in the stomach mucosal was established histopathologically. The use of morphine in the pretreatmant of indomethacin induced stress statistically significantly reduced the activity of all enzymes in the stomach compared to the control group, and this activity of catalase (CAT), glutathione peroxidase (GSHPx) and glutathione reductase (GR ), xanthine oxidase (XOD),as well as the lipid peroxidation intensity (Lpx), while the reduced glutathione content remained unchanged. Gastroprotective morphine activity in animals exposed to indomethacin induced stress is most likely a consequence of the strengthening of cytoprotective mechanisms rather than antioxidant action.

Newly synthetized derivative of bile acid, sodium salt of 3α, 7α-dihydroxy-12-oxo 5β cholanic acid (monoketocholanate) expressed a good characteristic as intranasal transport enhancer of xenobiotics.The aim of our sudy was to explore if it has an influence on bile metabolism and to measure its concentration in blood and bile after intravenous and intranasal administration. The experiment was performed in vivo on adult male Wistar rats. The determination of monoketocholanate (MKCh) in rats blood and bile, was carried out by high-performance liquid chromatography (HPLC), on an HP ODS2 column, using methanol/acetonitrile/acetate buffer as mobile phase. Absorbances were measured at 210 nm.Blood samples were taken from the prepared right axillary artery in 0, 1, 5, 10, 20, 30, 60, 90, 120 and 180 minutes from the beginning of the experiment. Bile was collected in a half an hour intervals,during the three hour period. The results showed that MKCh changed the amount of excreted bile depending on the way of application. Intranasal application increased the bile volume and the MKCh concentration, both in blood and bile compared to the intravenous application (p<0.05). Distributionm of MKCh through animal organism depends on the way of application of the substance, which probably determines its caracterisation as the transport promotor of applied xenobiotics. HPLC has proved as aa relatively simple, fast and effective method for the determination of synthetic bile acid,MKCh in these biological materials.

It is well known that there is a relationship between the zinc and diabetes, and its antioxidant potential. Based on that, the aim of this paper is to investigate the effects of different doses of zinc (9,2 and 18,4 mg / day) in combination with metformin and glibenclamide, to the total antioxidant status (TAS) and the activity of the enzyme superoxide dismutase (SOD) in experimentally-induced diabetic rabbits. The study was conducted on 24 New Zealand rabbits of both sexes, body weight 2,5 to 3,2 kg. In rabbits, experimental diabetes was induced i.v. injection of alloxan (80 mg / kg body weight). Three weeks after causing diabetes, the animals were divided into two groups: first group was treated oral with metformin, an appropriate dose (120 mg / kg body weight), while the second group of rabbits was treated with a suitable dose of glibenclamide (0,6 mg / kg BW). After the washout period (10 t1/2), the rabbits were treated with metformin and a first dose of zinc (9,2 mg) combination, i.e. glibenclamide and zinc (9,2 mg). After another washout period (10 t1/2) the rabbits were treated with metformin and a second dose of zinc (18,4 mg) combination, i.e. of glibenclamide and zinc (18,4 mg). Blood samples were taken in a specified time interval. The TAS value was significantly increased after administration of metformin, single and in combination with zinc, in doses of 9,2 and 18,4 mg, with respect to the value recorded before their application (p <0.05). Also, it is noted a significantly increased SOD activity after administration of metformin (i.e., glibenclamide), and zinc in combination, in a dose of 18,4 mg (p <0.05). This indicates that zinc and metformin have a significant positive effects on the parameters of antioxidative status, but with glibenclamide this effect did not occur.