Yazar "Akpolat, M" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Involvement of NMDA receptors and nitric oxide in the thermoregulatory effect of morphine in mice
    (Springer-Verlag Wien, 2000) Ulugol, A; Dost, T; Dokmeci, D; Akpolat, M; Karadag, CH; Dokmeci, I
    Morphine has long been known to have potent effects on body temperature. It has been suggested that both N-methl-D-aspartate (NMDA) receptors and nitric oxide (NO) pathway are involved in thermoregulation and also known to play important roles in some of morphine effects. The aim of this study was therefore to investigate the contribution of NMDA receptors and NO to the thermoregulatory effect of morphine. Morphine produced a hypothermic effect, especially at the dose of 10 mg/kg. Ketamine (5-40 mg/kg, i.p.) and N-G-nitro-L-arginine-methyl ester (L-Name, 1-100 mg/kg i.p.) also produced hypothermic effects with their higher doses. At doses which themselves produced no effect on colonic temperature in mice, both ketamine (10 mg/kg, i.p.) and L-NAME (10 mg/kg, i.p.) enhanced the hypothermic effect of morphine (10 mg/kg i.p.). These results further support the relationship between NO and NMDA receptors and suggest a possible role of NMDA-NO pathway in the thermoregulatory effect of morphine.
  • Küçük Resim Yok
    Öğe
    L-carnitine inhibits ethanol-induced gastric mucosal injury in rats
    (Springer Heidelberg, 2005) Dokmeci, D; Akpolat, M; Aydogdu, N; Doganay, L; Turan, FN
    L-carnitine is a quaternary amine that is essential for the normal oxidation of long-chain fatty acids by mitochondria. It is known that L-carnitine and its derivatives prevent the formation of reactive oxygen species, scavenge free radicals and protect cells from peroxidative stress. Oxygen-derived free radicals and lipid peroxidation products play a critical role in the pathogenesis of ethanol-induced gastric mucosal injury. The aim of the present study was to determine the effect of L-camitine on lipid peroxidation induced by ethanol in the rat stomach. In our study, gastric mucosal injury was induced by the intragastric administration of 1 ml of absolute ethanol. Test compounds were given to rats by gavage 30 min before the ethanol administration. The animals were killed 60 min after the administration of ethanol. The stomach of each animal was removed. Mucosal damage was evaluated by macroscopic examination, histological analysis and by measurement of lipid peroxidation and glutathione activity. The intragastric administration of ethanol induced hyperemia and hemorrhagic erosions in the rat stomachs. L-camitine significantly prevented gastric ulcerogenesis induced by ethanol and decreased the ulcer index. Plasma and gastric lipid peroxidation that was increased significantly by ethanol was decreased after treatment with L-camitine. Ethanol treatment decreased significantly the gastric glutathione levels, and pretreatment with L-camitine increased them significantly. Based on these data, the beneficial effects of L-camitine on ethanol-induced gastric mucosal injury may be attributed to its antiperoxidative effects.