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Öğe Amikacin ototoxicity enhanced by Ginkgo biloba extract (EGb 761)(Elsevier Science Bv, 2002) Miman, MC; Ozturan, O; Iraz, M; Erdem, T; Olmez, EAn animal study was realized to investigate the possible beneficial effect of EGb 761 as an antioxidant agent on amikacin ototoxicity by measuring distortion product otoacoustic emissions (DPOAEs). Twenty-eight adult rats were grouped equally as follows. Group amikacin: rats received amikacin 600 mg/kg/day intramuscularly between postnatal days (PND) 30 and PND44. Group amikacin/EGb 761: rats received amikacin 600 mg/kg/day intramuscularly between PND30 and PND44 and EGb 761 100 mg/kg/day orally between PND30 and PND50. Group EGb 761: rats received equivolume saline intramuscularly between PND30 and PND44 and EGb 761 100 mg/kg/day orally between PND30 and PND50. No treatment group: rats received nothing, Group amikacin was found to be affected only on the last measurement day of study (PND57). The frequencies greater than 2002 Hz were significantly reduced compared with the amplitudes of PND30 (P < 0.05). Group amikacin/EGb 761 was most and earliest affected by amikacin-induced ototoxicity. DPOAE amplitudes were found in this group to be decreased at 2-6 kHz starting on PND50. The results of Group EGb 761 and No treatment group were not significantly changed. For the DPOAE input/output amplitude thresholds, Group amikacin (P < 0.05) and Group amikacin/EGb 761 (P < 0.01) had significantly elevated thresholds on PND57, except at 5 kHz for Group amikacin (P = 0,06), According to the results of the study, EGb 761 may be regarded as a facilitating drug for the development of amikacin ototoxicity. The results of the present study may warn against concomitant use of aminoglycosides, specifically amikacin, with EGb 761. (C) 2002 Elsevier Science B.V. All rights reserved.Öğe 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, ESepsis 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.Öğe Determination of the pericardial to serum myoglobin ratio for the early diagnosis of perioperative myocardial infarction after coronary artery bypass grafting(Academic Press Ltd Elsevier Science Ltd, 2004) Cihan, HB; Gulcan, O; Hazar, A; Turkoz, R; Olmez, EPericardial fluid reflect the composition of cardiac interstitium in myocardial ischemia. This study investigated the value of the pericardial and serum myoglobin (MG) measurements for the diagnosis of perioperative myocardial infarction (MI) after coronary artery bypass grafting (CABG). Postoperative arterial and pericardial blood samples were taken in 64 subjects undergoing elective CABG allocated to two groups according to the 12-lead electrocardiogram (ECG) abnormalities observed during the first postoperative 24 It. Group 1=normal and nonspesific ECG abnormalities, and Group 2=perioperative Q-wave MI. The occurrence of perioperative MI was associated with a dramatic increase in both serum and pericardial cardiac troponin I (CTnI) and MG concentrations. Pericardial concentrations were higher than serum concentrations during the first postoperative 24 h in all subject. However, pericardial/serum CTnI ratio in subjects in Group 2 was not statistically different from Group I at the time of admission to the intensive care unit (ICU) and did not significantly change at time intervals. On the other hand, more than two-fold increase in the pericardial/serum MG ratio was determined for all patients who experienced perioperative Q-wave MI with the lowest value as 2.75, whereas only 1 of 59 patients in group 1 had the ratio higher than 2 with the highest value as 2.15 at the time of admission to the ICU. In conclusion, determination of pericardial/serum MG ratio may be a useful tool for the early diagnosis of the perioperative MI after CABG. (C) 2004 Elsevier Ltd. All rights reserved.Öğe Dose-dependent dual effect of melatonin on ototoxicity induced by amikacin in adult rats(Springer, 2005) Erdem, T; Ozturan, O; Iraz, M; Miman, MC; Olmez, EThe aim of this animal study was to reveal the dose-dependent effects of melatonin on aminoglycoside ototoxicity by utilizing distortion product otoacoustic emissions (DPOAEs). Forty-four adult ( aged 12 months) rats were divided into five groups. Rats of the control group ( group C) were injected with vehicle, while the melatonin group ( group M) received melatonin ( 4 mg/kg per day); there were four rats in each of these groups. The study groups consisted of 12 rats per group, and they were treated as follows: 600 mg/kg per day amikacin ( group A), amikacin plus a low dose (0.4 mg/kg per day) melatonin ( group AML) and amikacin plus high dose ( 4 mg/kg per day) melatonin ( group AMH) for 14 days. During the serial measurements on days 0, 5, 10 and 15, the DPOAE results of groups C, M and AML were not significantly changed. Amikacin ototoxicity findings for input/output (I/O) functions were detected on the 3rd measurement of the study in group A. High-dose melatonin clearly enhanced and accelerated amikacin-induced ototoxicity. The DP-gram amplitudes and I/O amplitudes were reduced, and I/O thresholds were increased in group AMH. Group AMH was the group that was affected the most and earliest by amikacin. Our study results showed that while low-dose melatonin protected the inner ear from ototoxicity, high dose melatonin facilitated amikacin-induced ototoxicity, possibly via the vasodilatory effect, leading to an increased accumulation of amikacin in the inner ear. Probably, the protective effect of the melatonin at a dose of 0.4 mg/kg per day is related to its antioxidant properties. Apparently, the vasodilatory effect of melatonin seems to be more prominent than its antioxidant effect in high doses.Öğe Effects of captopril on ischaemia-reperfusion-induced arrhythmias in an in vivo rat model(Academic Press Ltd, 1995) Olmez, E; Birincioglu, M; Aksoy, T; Acet, AThe antiarrhythmic effects of captopril, an angiotensin converting enzyme (ACE) inhibitor, were investigated in an in vivo rat model of coronary artery ligation. Captopril (0.3-3 mg kg(-1)) or saline were administered by intravenously 10 min before coronary ischaemia. The left main coronary artery was then occluded for 7 min, followed by 7 min of reperfusion. Captopril caused a marked decrease in mean arterial blood pressure which was transient at 0.3 and 1 mg kg(-1), and at doses of 1 and 3 mg kg(-1), it produced marked bradycardia. The incidence of ventricular tachycardia (VT) on ischaemia was significantly reduced the captopril at a dose of 3 mg kg(-1) only and on reperfusion at doses of 1 and 3 mg kg(-1). At the same doses, captopril significantly reduced the mean duration of ventricular fibrillation (VF) on reperfusion. The incidence of mortality resulting from reperfusion-induced irreversible VF in the control group decreased from 42.9% to 14.3% (NS), 21.4% (NS) and 7.7% (P<0.05) in captopril at 0.3, 1 and 3 mg kg(-1), respectively. Our results indicate that captopril appears to limit the arrhythmias following reperfusion and this may be due in part to the antiischemic effect associated with bradycardia and vasodepression. (C) 1995 The Italian Pharmacological SocietyÖğe 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, EThe 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.Öğe The effects of estrogen/progesterone replacement therapy with or without low-dose testosterone on ischemia-reperfusion induced ventricular arrhythmias in ovariectomized rats.(Elsevier Science Inc, 1997) Taskin, O; Birincioglu, M; Olmez, E; Aksoy, T; Kilic, E; Wheeler, JM[Abstract Not Available]Öğe Effects of physiological and pharmacological concentrations of melatonin on ischemia-reperfusion arrhythmias in rats: can the incidence of sudden cardiac death be reduced?(Wiley, 2002) Sahna, E; Olmez, E; Acet, ACardiac arrhythmias during ischemia-reperfusion (I/R) are believed to be related to free radicals generated in the heart especially during the period of reperfusion. The pineal secretory product. melatonin, is known to be a potent free radical scavenger and its pharmacological concentrations have been shown to reduce the I/R-induced arrhythmias in isolated rat hearts. However, the physiological role of melatonin in the prevention of these arrhythmias is unknown. Rats were pinealectomized (Px) or sham-operated (non-Px) (control) 2 months before the I/R studies. To produce arrhythmias. left main coronary artery was occluded for 7 min, followed by 7 min reperfusion, in anesthetized rats. The incidence of mortality resulted from irreversible ventricular fibrillation (VF) was found significantly higher in the Px rats (63%) than in the control group (25%). Melatonin administration (0.4 mg,kg, either before ischemia or reperfusion) to Px rats significantly reduced the incidence of total (irreversible plus reversible) and irreversible VF and returned them to control values. On the other hand, melatonin administration (0.4 and 4 mg/kg) to non-Px rats failed to attenuate the I/R arrhythmias, significantly. These results suggest that physiological melatonin concentrations are important to reduce the I/R-induced VF and mortality. while pharmacological concentrations of melatonin did not increase its beneficial effect on these arrhythmias. As melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate the incidence of sudden cardiac death especially in older patients,Öğe Melatonin attenuates ?-adrenergic-induced contractions by increasing the release of vasoactive intestinal peptide in isolated rat penile bulb(Springer, 2003) Olmez, E; Kurcer, ZThe 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.Öğe Myocardial and electrocardiographic findings in fatal carbon monoxide poisoning: An experimental study(Elsevier Sci Ireland Ltd, 2003) Mizrak, B; Celbis, O; Olmez, E; Iraz, M[Abstract Not Available]Öğe Myocardial ischemia-reperfusion in rats: reduction of infarct size by either supplemental physiological or pharmacological doses of melatonin(Wiley, 2002) Sahna, E; Acet, A; Ozer, MK; Olmez, EMyocardial ischemia reperfusion (I/R) represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. I/R injury is believed to be a consequence of free radical generation in the heart especially during the period of reperfusion. The pineal secretory product, melatonin, is known to be a potent free radical scavenger and pharmacological concentrations have been shown to reduce the I/R-induced cardiac damage in isolated rat hearts. However, the physiological role of melatonin in the prevention of this damage is unknown. Rats were pinealectomized or sham-operated (control) 2 months before the I/R studies. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 in reperfusion, in anesthetized rats. Infarct size, expressed as the percentage of the risk zone, was found significantly higher in pinealectomized rats (49 +/- 4%) than in the control group (34 +/- 6%). Melatonin administration (4 mg/kg, either before ischemia or reperfusion) to pinealectomized rats significantly reduced the infarct size values and returned the to the control values. On the other hand, melatonin administration (4 mg/kg) to sham-operated rats failed to attenuate significantly the I/R-induced infarct size. These results suggest that physiological melatonin concentrations are important in reducing the I/R-induced myocyte damage, while pharmacological concentrations of melatonin did not add to the beneficial effect. As melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate I/R-induced myocardial injury, especially in older patients.Öğe Protective effect of ACE inhibitors on ischemia-reperfusion-induced arrhythmias in rats: Is this effect related to the free radical scavenging action of these drugs?(Harwood Acad Publ Gmbh, 1997) Birincioglu, M; Aksoy, T; Olmez, E; Acet, AThe antiarrhythmic effects of captopril, a sulphydryl-containing angiotensin converting enzyme (ACE) inhibitor, were compared with those of the non-sulphydryl-containing ACE inhibitor Lisinopril and the sulphydryl-containing agent glutathione in an in vivo rat model of coronary artery ligation. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion. Captopril (3 mg kg(-1)) and lisinopril (0.1, 0.3 or 1 mg kg(-1)) caused marked decreases in mean arterial blood pressure (BP) and heart rate, whereas glutathione (5 mg kg(-1)) had no effect on them. The incidence of ventricular tachycardia (VT) on ischemia and reperfusion was significantly reduced by captopril and lisinopril. Captopril and 1 mg kg(-1) lisinopril also significantly decreased the number of VEB during occlusion and the duration of VT on reperfusion, respectively. These drugs also attenuated the incidence of reversible ventricular fibrillation (VF) and the number of ventricular ectopic beats (VEB) during reperfusion. However, glutathione only reduced the incidence of VT on reperfusion, significantly. These results suggest that, in this experimental model, ACE inhibitors limit the arrhythmias following ischemia-reperfusion and free radical scavenging action of these drugs does not have a major contributory role in their protective effect.Öğe The role of prostaglandin synthesis stimulation in the protective effect of captopril on ischaemia-reperfusion arrhythmias in rats in vivo(Academic Press Ltd, 1997) Birincioglu, M; Olmez, E; Aksoy, TA; Acet, AAttenuation of ischaemia-reperfusion induced arrhythmias by several angiotensin converting enzyme (ACE) inhibitors, such as captopril, has been demonstrated. The role of prostaglandin synthesis stimulation in this protective effect of ACE inhibition was evaluated in an in vivo rat model. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion. Captopril (3 mg kg(-1)) and a prostaglandin synthesis inhibitor, indomethacin (2 mg kg(-1)) alone or together were administered by intravenous (i.v.) injection 10 min before occlusion. Captopril reduced the incidence of ventricular tachycardia (VT) and the number of ventricular ectopic beats (VEE) on ischaemia and reperfusion as well as the incidence of reversible ventricular fibrillation (VF) on reperfusion. These protective effects of captopril against ischaemia-reperfusion-induced arrhythmias were prevented by indomethacin. Captopril also caused a sustained decrease of preocclusion values in the arterial blood pressure (BP) and heart rate (HR), whereas in the presence of indomethacin, captopril had no significant effect on either HR or arterial BP values except the heart rate value just before occlusion. Indomethacin alone did not affect either the severity of arrhythmias or the haemodynamic parameters. These results suggest that, in this experimental model, the protective effects of ACE inhibitors on the arrhythmias following ischaemia-reperfusion are mediated by the stimulation of prostaglandin synthesis and the haemodynamic effects of these drugs may have a contributory role in their protective effect. (C) 1997 The Italian Pharmacological Society.
