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T Celik

Publications and source records attributed to T Celik.

17 recordsLinked to original sources
PubMed2004

Spironolactone does not prevent restenosis after coronary stenting in humans.

INTRODUCTION: In animal studies, aldosterone enhanced neointimal proliferation by increasing extracellular accumulation of collagen and potentiating the effects of angiotensin II. Spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal proliferation. We conducted a placebo-controlled, double-blind, randomised study to assess the effect of spironolactone on angiographic 6-month in-stent restenosis. MATERIALS AND METHODS: Of the 310 randomised patients with significant coronary artery disease, 258 patients were available for analysis: 128 constituted the placebo group and 130 were assigned to receive spironolactone. Eligible patients were randomly assigned to receive a dose of 50 mg spironolactone or placebo orally twice a day for 6 months. The primary endpoint was the angiographic restenosis (>50% stenosis) rate at follow-up angiography. RESULTS: At 6-month follow-up angiography after stenting, there was no difference between the 2 groups in minimal lumen diameter, percent diameter stenosis, late loss, and net gain. Angiographic restenosis occurred in 46 (35.4%) of 130 patients receiving spironolactone and 50 (39.0%) of 128 in the placebo group with an odds ratio (OR) of 0.85 with a 95% confidence interval (CI) of 0.49 to 1.46 (P = 0.62). Restenosis rate was found in 60 (32.9%) of 182 lesions in the spironolactone group, and 61 (35.5%) of 172 lesions in the placebo group with an OR of 0.89 with a 95% CI of 0.56 to 1.42 (P = 0.89). CONCLUSIONS: Spironolactone did not reduce the incidence of in-stent restenosis as compared with placebo in human, contrary to the fact that reduction of neointimal formation in animal models has been observed upon administration of spironolactone.

Adult↗
PubMed2002

Salbutamol intoxication: is salbutamol a drug-inducing fever? A case report and treatment strategy.

A four-year-old female with salbutamol intoxication was referred to our paediatric emergency medicine unit, due to agitation, tremulousness, sinus tachycardia, mild hypokalaemia and hyperglycaemia. On admission the child was agitated and had a noticeable tremor, an axillary temperature of 38 degrees C and a pulse rate of 185 beats/min. She had no identifiable focus of infection on physical examination to explain her fever. Gastric lavage, activated charcoal, intravenous hydration and electrocardiogram (ECG) monitoring were performed. Her plasma potassium level, blood sugar and QT interval were closely monitored during her hospital stay. Her fever, tachycardia and serum potassium and glucose levels returned to normal and she was discharged in good condition 24 h after admission. The difference of this case from prior cases of salbutamol intoxication was the observation of fever in the absence of evidence of infection. Since the cause of fever was not a reaction to the medication used in the treatment or related to environmental factors, it is assumed that salbutamol is a fever-inducing drug.

Albuterol↗
PubMed2000

Effects of agmatine on ethanol withdrawal syndrome in rats.

Effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, have been investigated on the ethanol withdrawal syndrome in rats. Adult male Wistar rats were used in the study. Ethanol (7.2% v/v) was given to the rats by a liquid diet for 21 days. Agmatine (20, 40, 80 and 160 mg/kg) and saline were injected to rats intraperitoneally 30 min before ethanol withdrawal testing. After 30th min, 2nd and 6th h of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs which included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes and tremor were recorded or rated. A second series of injections was given at 6 h after the first one, and subjects were then tested for audiogenic seizures. Agmatine caused dose-dependent and significant inhibitory effects on stereotyped behaviors, wet dog shakes and tremors during the observation period. It did not cause any significant change in motor coordination of naive (not ethanol-dependent) rats. Our results suggest that agmatine attenuates withdrawal syndrome in ethanol-dependent rats; thus, this drug may be beneficial in the treatment of ethanol dependence.

Agmatine↗
PubMed1999

Nitric oxide synthase inhibition blocks amphetamine-induced locomotor activity in mice.

Effects of N(G)-nitroarginine methyl ester (L-NAME), a nonspecific inhibitor of nitric oxide (NO) synthase, on amphetamine-induced locomotor activity were investigated in Swiss-Webster mice. Locomotor activity was measured for 30 min immediately following amphetamine (1, 2 and 4 mg/kg, i.p.) or saline treatments. L-NAME (15 and 30 mg/kg) and a combination of L-arginine (1000 mg/kg) and L-NAME (30 mg/kg) were injected 30 min before amphetamine (2 mg/kg) to other groups of the mice. L-Arginine was injected 30 min before L-NAME treatment when they were combined. L-NAME (30 mg/kg) and L-arginine (1000 mg/kg) were also tested for ability to depress or stimulate locomotor activity in the absence of amphetamine. Amphetamine caused a dose-dependent increase in locomotor activity of the mice. L-NAME blocked the amphetamine-induced locomotor stimulation dose dependently. L-Arginine pretreatment prevented the inhibitory effects of L-NAME on amphetamine-induced locomotor stimulation. L-NAME and L-arginine did not cause any significant change in locomotor activity in mice not treated with amphetamine. These results suggest that amphetamine-induced locomotor stimulation in mice is modulated by NO.

Amphetamine↗
PubMed1999

Combination treatment of hepatic encephalopathy due to thioacetamide-induced fulminant hepatic failure in the rat with benzodiazepine and opioid receptor antagonists.

BACKGROUND/AIMS: Treatment of hepatic encephalopathy with drugs acting on the target organ of this syndrome, the brain, is unsatisfactory. Combination treatment with different neurotransmitter receptor antagonists may be a rational option to optimize treatment. METHODS: The effects of various doses of the benzodiazepine receptor antagonist Ro 15-3505 and the opioid receptor antagonist naloxone, alone or in combination, were tested on hepatic encephalopathy in rats with thioacetamide-induced hepatic failure in an open-field activity meter. Comparison of single and combination treatment was also done using a neurological test battery. In addition, we compared survival of treatment-responder rats with treatment non-responders. RESULTS: Naloxone dose dependently increased ambulatory activity and improved neurological score. Ro 15-3505 also improved ambulatory activity and neurological score; however, the improvement was less evident at higher doses. Combination treatment was not superior to single treatment. Survival was increased in treatment-responder rats. CONCLUSIONS: The failure of combination treatment with Ro 15-3505 and naloxone to further improve hepatic encephalopathy may suggest that the two neurotransmitter systems are interrelated or that hepatic encephalopathy may not be further improved by drugs acting on the brain.

Animals↗
PubMed1999

The effects of flumazenil on two way active avoidance and locomotor activity in diazepam-treated rats.

The present study was undertaken to determine the effects of chronic flumazenil treatment alone and simultaneously with diazepam on acquisition performance in an active-avoidance task and on locomotor activity in rats. Flumazenil (5, 10 and 20 mg/kg) and diazepam (0,5, 1.0 and 2.0 mg/kg) were administered intraperitoneally to rats before each daily training session for 5 days. The baseline of avoidance performance was set to approximately 50% and responses were expressed as acquisition rate. Locomotor activity of the rats was simultaneously recorded but only following the first training session. Diazepam decreased acquisition rate between the dose range used. Flumazenil had no effect on the acquisition rate of naive rats but reversed low dose diazepam-induced learning and memory impairment. Diazepam induced locomotor depression within the same dose range that decreased acquisition rate. Flumazenil had no effect on locomotor activity, but reversed the locomotor depressant effect of diazepam. The striking contradiction with previous data that flumazenil has no effect on learning-memory processing is discussed.

Animals↗
PubMed1998

Opioid receptor ligands in human hepatic encephalopathy.

BACKGROUND/AIMS: Opioid peptides may contribute to some of the manifestations of hepatic encephalopathy. To address the role of the opioid system in the pathogenesis of hepatic encephalopathy, three representative opioid ligands were measured in plasma and cerebrospinal fluid of patients with hepatic encephalopathy. METHODS: Plasma and cerebrospinal fluid were obtained in three groups of patients: group 1: patients with hepatic encephalopathy; group 2: patients with lumbar back pain; group 3: healthy controls. Met-enkephalin, leu-enkephalin and beta-endorphin levels were measured in extracted plasma and cerebrospinal fluid samples by radioimmunoassay. RESULTS: Plasma met-enkephalin levels were 656% (p<0.05) and 301% (p<0.05) and cerebrospinal fluid met-enkephalin levels were 1481% (p<0.01) and 645% (p<0.05) higher when compared to healthy control and pain control patients, respectively. Although plasma and cerebrospinal leu-enkephalin levels were elevated in patients with hepatic encephalopathy, the increases were not statistically significant. Plasma and cerebrospinal beta-endorphin levels were similar in the three study groups. CONCLUSIONS: The results of this study support accumulating data on the role of the delta opioid receptor ligand met-enkephalin in the pathogenesis of hepatic encephalopathy, and provide a rationale for the use of opioid receptor antagonists in the treatment of hepatic encephalopathy.

Enkephalin, Leucine↗
PubMed1995

Investigation of the effects of moclobemide in chronic ethanol feeding rats.

Effects of chronic moclobemide administration on ethanol consumption, blood ethanol level, motor coordination and seizures induced by an audiogenic stimulus during ethanol withdrawal syndrome have been investigated in chronically ethanol intoxicated rats. Adult male Wistar rats (211-289 g) were used. Ethanol (7.2% v/v) was given to rats by a special liquid diet for 15 days. Moclobemide (10, 30 and 45 mg kg-1) or saline was injected to ethanol-feeding rats subcutaneously through 15 days. Daily ethanol intake and body weight gain of the rats were recorded. Blood ethanol levels were measured in rats given saline or chronic moclobemide (30 mg kg-1) just before and 6 h after ethanol withdrawal. At the sixth hour of the ethanol withdrawal, the incidence, intensity and latency of the seizures induced by an audiogenic stimulus were recorded in saline and acute (30 mg kg-1) or chronic (10, 30 and 45 mg kg-1) moclobemide-administered rats. Accelerod performances of the chronic moclobemide (45 mg kg-1) or saline injected rats were also evaluated. The mean ethanol intake of the rats ranged from 10.06 to 15.63 g kg-1 day-1 during the study. Chronic moclobemide treatment did not occur any significant effect on daily ethanol consumption, ethanol clearance and accelerod performances of the rats. No significant changes on the incidence, intensity and the latency of the audiogenic seizures were also observed. Our results suggest that there has been no adverse interaction between ethanol and moclobemide.

Alcohol Drinking↗
PubMedDate not supplied

Wellens' syndrome: a case report.

The pattern of clinical findings and electrocardiography (ECG) changes known as Wellens' syndrome is associated with significant stenosis of the proximal left anterior descending coronary artery. Cases can be classified according to the ECG pattern into type 1 (biphasic T waves) or type 2 (deeply inverted T waves, especially in leads V2 and V3). We present here an unusual case of Wellens' syndrome in which the ECG pattern changed from type 2 to type 1 during observation, and in which the coronary lesion was in the middle rather than the proximal part of the left anterior descending artery.

Coronary Angiography↗
PubMedDate not supplied

Assessment of interventricular septal motion using colour tissue Doppler imaging in adult patients with atrial septal defect.

We aimed to characterize changes in interventricular septum (IVS) motion and any relationship between them and the pulmonary-to-systemic flow ratio (Qp/Qs) in adult patients with atrial septal defect (ASD). Patients and controls were studied using colour tissue Doppler imaging (TDI). The septum length (SL) and distance from the colour change point (CCP) on the IVS to the aortic valve (the CCP distance) were measured on parasternal long axis views. Values normalized for body surface area, and the CCP distance to SL ratio, were calculated. Qp/Qs values were correlated with CCP distance, normalized CCP distance and CCP distance:SL ratio. Statistically significant differences in CCP distance, normalized CCP distance and CCP distance:SL ratio were found between the two groups. In the ASD group, there was no correlation between Qp/Qs and the echocardiographic measurements. The point between the motions in two different directions from the IVS shifted toward the apex in ASD patients compared with controls, and may be a mechanism involved in paradoxical septal motion.

Adult↗
PubMedDate not supplied

Echocardiographical characteristics of healthy young subjects with physiological mitral regurgitation.

We aimed to analyse the echocardiographical characteristics of healthy subjects and determine the causal mechanism of the development of physiological mitral regurgitation (PMR). A total of 130 healthy subjects were divided into two groups according to whether or not PMR was detected. There were no statistical differences between the two groups in terms of the mean values of the systolic and diastolic left ventricular internal diameters and the left atrial diameter. The mean values of the length and thickness of the anterior mitral valve (AMV) and the mitral annular diameter (MAD) from subjects in group 1 (with PMR) were statistically different from those of group 2 (without PMR). In conclusion, the AMV was slightly longer and thicker and the MAD was smaller in subjects with PMR than in subjects without PMR. The changes observed in the AMV and the mitral annulus may play a causal role in the development of PMR.

Adolescent↗