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    Beneficial effects of melatonin on diaphragmatic contractility and fatigability in Escherichia coli endotoxemic rats
    (Georg Thieme Verlag Kg, 2006) Kurcer, Z; Iraz, M; Kelesyilmaz, N; Kilic, N; Olmez, E
    Sepsis impairs diaphragmatic contractility and endurance capacity and increases diaphragmatic fatigability. Several investigations have shown that administration of a number of free radical scavengers, such as N-acetylcysteine (NAC), protects the diaphragm from the development of endotoxin-mediated diaphragmatic dysfunction. The aim of this study was to evaluate the effects of melatonin (CAS 73-31-4), a naturally occurring potent antioxidant, on diaphragmatic contractility and lipid peroxidation as a marker of oxidative stress in endotoxemic rats. Rats were randomly divided into four groups: control group, endotoxemic group, melatonin group and endotoxemic plus melatonin group. Melatonin was administered by intraperitoneal injection 30 min before endotoxin inoculation to animals. Diaphragmatic function and malondialdehyde (MDA) level analysis as an indicator of lipid peroxidation were assessed 17 h after endotoxin or saline inoculation. Endotoxemia decreased the tensions generated in response to all frequencies of stimulation and increased the development of diaphragm fatigue and diaphragmatic MDA levels. The effects of endotoxemia on diaphragmatic contractions and fatigability were reversed and returned to control levels by melatonin administration. However, melatonin did not prevent the increase in muscle MDA content. In conclusion, the present study demonstrated that melatonin attenuated the endotoxin-induced impairment of diaphragm function. This effect of melatonin does not seem to be related to its antioxidant properties.
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    Effects of chronic ethanol consumption on ?-adrenergic-induced contractions and endothelium-dependent relaxations in rat thoracic aorta
    (Academic Press Ltd, 2000) Sahna, E; Kurcer, Z; Ozturk, F; Cengiz, N; Vardi, N; Birincioglu, M; Olmez, E
    The effects of chronic oral administration of ethanol (7.2% daily during 24 weeks) on the contractions induced by phenylephrine (Phe) and the endothelium-dependent relaxation responses to acetylcholine (ACh) were studied in rat thoracic aorta. Ethanol pretreatment significantly attenuated the contractile responses to Phe, resulting in parallel shift of the concentration-response curve to the right. EC50 values of Phe were 64.6 +/- 11.2 and 95.5 +/- 8.5 nmol l(-1) in control and ethanol-fed rats, respectively. On the other hand, either calcium-induced contractions or relaxation responses to ACh and sodium nitroprusside were similar in the vessels of the control and ethanol-treated rats. These results suggest that chronic ethanol ingestion significantly attenuates the alpha(1)-adrenergic-induced contractions but does not affect the relaxation responses mediated by nitric oxide in rat aortic rings. (C) 2000 Academic Press.
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    Melatonin attenuates ?-adrenergic-induced contractions by increasing the release of vasoactive intestinal peptide in isolated rat penile bulb
    (Springer, 2003) Olmez, E; Kurcer, Z
    The effects of melatonin on alpha-adrenergic-induced contractions caused by electrical field stimulation (EFS) or the alpha(1)-adrenoceptor agonist phenylephrine (Phe) were investigated in isolated rat penile bulb. Melatonin as well as melatonin receptor agonists N-acetylserotonin and 2-iodomelatonin and melatonin antagonist luzindole attenuated the EFS-induced contractions and the concentration-response curve to Phe. The effect of melatonin on Phe-induced contractions was completely reversed by treatment with tetrodotoxin, guanethidine or vasoactive intestinal peptide (VIP) antagonist. On the other hand, pretreatment with N-methyl-l-arginine, atropine, and luzindole did not reverse the effect of melatonin. Thus, we demonstrated that melatonin at nanomolar concentrations inhibits the alpha-adrenergic responses in isolated rat penile bulb. Since alpha-adrenoceptor blocking agents are known to interfere with detumescence of the erect penis, serum levels or administration of this pineal hormone may affect erectile function. This effect of melatonin may be the result of its allosteric interaction with the presynaptic receptors on VIPergic neurons, which are affected by sympathetic transmission, and then an increase in VIP release from these neurons.