Biomedical subjects

Y Tuncok

Publications and source records attributed to Y Tuncok.

At least 19 recordsLinked to original sources

PubMed2006

A retrospective analysis of antidepressant poisonings in the emergency department: 11-year experience.

Between 1993 and 2004, patients with antidepressant poisoning admitted to an emergency department (ED) were analysed retrospectively with regard to demographics, clinical findings and treatment attempts. Age, gender, suicide attempts, classification of antidepressants, Glasgow Coma Scale (GCS) score, ECG findings, need for endotracheal intubation, follow-up period and Antidepressant Overdose Risk Assessment (ADORA) criteria were analysed by SPSS software. A total of 356 antidepressant poisoning cases were evaluated. Tricyclic antidepressants (TCA), especially opipramol and amitriptyline, were the most common agents (58.4%). The most frequent ECG finding was sinus tachycardia (40.7%, n=145). Endotracheal intubation was required in 9.6% of cases. Patients with TCA ingestion had a longer observation time in the ED, abnormal ECG findings, abnormal physical examination findings and more ADORA criteria, than patients who ingested selective serotonin re-uptake inhibitors (SSRI) (P = 0.008, P = 0.008, P < 0.001, P < 0.001). It was found that the patients who ingested TCA (P = 0.001), poisoned with amitriptyline (P = 0.001), patients with GCS scores of 8 and less (P = 0.001), patients with two or more ADORA criteria (P = 0.001), with seizures (P = 0.001), with abnormal ECG (P = 0.012), and patients with a history of two or more suicide attempts were intubated more frequently. Suicide attempts, classification of the antidepressant, ECG findings, seizure, GCS score and number of detected ADORA criteria affect the need for intubation in patients with antidepressant poisoning.

Adolescent↗

PubMed2005

Efficacy of an adenosine A1 receptor agonist compared with atropine and pralidoxime in a rat model of organophosphate poisoning.

The objective of this study was to evaluate the effects of an adenosine A1 agonist, phenylisopropyl adenosine (PIA), on metamidophos poisoning compared to specific antidotes. Rats were poisoned with metamidophos (30 mg/kg, oral) and observed for 24 hours. One group received sodium chloride (1 mL/kg) and four experimental groups received atropine (5 mg/kg), pralidoxime (PAM, 20 mg/kg), atropine/PAM (5/20 mg/kg) or PIA (1 mg/kg) intraperitoneally. Atropine reduced salivation and prevented respiratory distress when compared to sodium chloride-treated rats. Treatment with PAM did not cause any suppression of cholinergic signs. Atropine and PAM combination prevented salivation, convulsion and respiratory distress. PIA delayed initial time of the salivation, convulsion and time to death. However, PIA was found ineffective against the metamidophos-induced cholinergic symptoms and mortality. All treatments, except PIA, lead to survival of these animals. Acetylcholinesterase (AChE) activity was not normalized by PIA or PAM. PIA prevented metamidophos-induced diaphragmatic muscle necrosis as much as PAM. In conclusion, a single dose of PIA was unable to protect the rats from metamidophos toxicity. Further studies are needed involving a combination of PAM and/or atropine with repeated doses of PIA to clarify the efficacy of adenosine agonists in OP poisoning.

Adenosine A1 Receptor Agonists↗

PubMed2001

Inhibition of nicotine-induced seizures in rats by combining vaccination against nicotine with chronic nicotine infusion.

The ability of a nicotine vaccine to protect against nicotine-induced seizures was studied in rats. Groups of 10 rats were vaccinated with 3 doses of either a nicotine conjugate vaccine over 6 weeks to elicit high titers of nicotine-specific antibodies or with a control vaccine. Rats were then pretreated with a 1-week subcutaneous infusion of either nicotine 1 mg/kg/day or saline and then received a single 2 mg/kg ip dose of nicotine to provoke seizures. Vaccination reduced the incidence of seizures. The combination of vaccination and pretreatment with nicotine infusion was more effective than either treatment alone. These data suggest that vaccination is protective against this toxic effect of nicotine and that combining vaccination and chronic nicotine administration may provide a novel strategy for blocking some effects of nicotine.

Animals↗

PubMed2001

The effects of captopril on serum digoxin levels in patients with severe congestive heart failure.

The effects of captopril on serum digoxin concentrations were studied in 8 patients with severe (NYHA Class IV) congestive heart failure. Serum digoxin concentrations were determined before and after the administration of captopril for 1 week in patients on chronic digoxin therapy. Each patient who was taking 0.25 mg of digoxin PO q.d., was administered 12.5 mg of captopril PO t.i.d. for 7 days. The peak serum concentration of digoxin (Cmax) before and after (on Days 0 and 7) captopril administration was 1.7+/-0.2 ng/ml and 2.7+/-0.2 ng/ml, the time to peak (tmax) was 2.4+/-0.5 h and 1.3+/-0.2 h, and the area under the 24-hour digoxin concentration-time curve (AUC0-24h) was 30.0+/-1.5 ng x h/ml and 41.7+/-3.4 ng x h/ml, respectively. While captopril caused a significant increase in peak serum concentration and the area under the digoxin concentration-time curve, it decreased the time to digoxin peak (p = 0.01, p = 0.04, p = 0.01, respectively). No patient developed evidence of digoxin toxicity. Concomitant administration of captopril with digoxin increases serum digoxin concentration in patients with severe congestive heart failure.

Administration, Oral↗

PubMed2001

Acute renal failure following latrodectism.

Latrodectism is considered dangerous for human beings. Acute renal failure after envenomation is not common and usually results from prerenal failure. We report a 59-y-o man with acute oliguric renal failure due to a combination of prerenal and renal causes after being bitten by a black Latrodectus spider. He had the characteristic anxiety, severe hypertension, tremor, facial edema, and generalized diaphoresis. The patient recovered within a week without sequelae. Clinicians should not overlook the possibility of acute renal failure in latrodectism.

Acute Kidney Injury↗

PubMed2000

The effects of propofol on normal and hypercholesterolemic isolated rabbit heart.

The aim of the present study was to compare the effects of propofol on cardiac contractile force in normal and hypercholesterolemic isolated rabbit hearts. While one group was fed with standard chow pellets (150 g/day), the other group received cholesterol (1% w/w) in addition to the same amount of rabbit chow pellets during 1 month. Hearts from standard-fed rabbits were given intralipid solvent or 25, 50 and 100 microM propofol by infusion. Hypercholesterolemic rabbit hearts were administered 25, 50 and 100 microM propofol by infusion. All concentrations of propofol did not result in any significant change of the heart rates (HR) in two groups. Propofol (25, 50 and 100 microM) infusion induced a concentration- and time-dependent inhibition in left ventricular pressure (LVP) in standard chow diet group (P<.05,.05 and.05, respectively). In hypercholesterolemic rabbit hearts, 25 and 50 microM propofol infusion developed a significant inhibition in LVP when compared with the standard chow diet group (P<.05 and.05, respectively). Propofol (100 microM) infusion developed a significant increase in LVP after 20 min in hypercholesterolemic rabbit hearts when compared with normal rabbit hearts (P<.05). Supratherapeutic concentration of propofol might have cardioprotective effect on hypercholesterolemic rabbit hearts.

Anesthetics, Intravenous↗

PubMed1999

Midazolams cardiac depressant effects and their lack of reversal by flumazenil in isolated rabbit hearts.

Midazolam is known to cause a dose-dependent increase and decrease in the contractile force of the myocardium. Whether flumazenil can reverse these effects of midazolam remains unclear. In this study, we determined the cardiac effects of midazolam and the counter effect of flumazenil on midazolam-induced myocardial depression in isolated rabbit hearts. Rabbit hearts were isolated and perfused using the Langendorff technique, and left ventricle pressure and heart rate were measured by a pressure transducer in the left ventricle. One set of hearts were perfused with increasing concentrations of midazolam for 10 min, another set were perfused with concomitant midazolam and flumazenil. Concentrations of 5, 10, 20 and 50 microM midazolam decreased left ventricle pressure significantly (P < 0.01, P < 0.05, P < 0.01, P < 0.01, respectively). Heart rates decreased with concentrations of 10, 20 and 50 microM midazolam (P < 0.01, P < 0.01, P < 0.05, respectively). Flumazenil had no effect on the midazolam-induced decrease in left ventricle pressure and heart rate. Midazolam decreased the cardiac contractile force and heart rate of isolated rabbit hearts in a concentration-dependent manner. The failure of flumazenil to reverse these effects suggest that this cardiac depressant effect of midazolam is not mediated through peripheral benzodiazepine receptors.

Anesthetics, Intravenous↗

PubMed1999

Severe uvular angioedema caused by intranasal administration of Ecbalium elaterium.

A 54-y-o woman presented to the Emergency Department with shortness of breath and sore throat after intranasal administration of Ecbalium elaterium as a folk remedy for her sinusitis. The patient's history included nasal aspiration of the juice of the squirting cucumber (Ecbalium elaterium) for acute maxillary sinusitis. An airway obstruction due to severe uvular angioedema was detected and confirmed by airway X-ray. The patient was treated with 100% oxygen with mask, 0.3 mg epinephrine s.c., and 80 mg prednisolone i.v. Renal and hepatic function tests were normal. After a 24-h observation, the patient was discharged in her previous state of health.

Administration, Intranasal↗

PubMed1998

The effects of 4-aminopyridine and Bay K 8644 on verapamil-induced cardiovascular toxicity in anesthetized rats.

OBJECTIVE: To determine the effects of 4-aminopyridine and Bay K 8644 on mean arterial pressure and heart rate in an anesthetized rat model of verapamil toxicity. METHODS: The study was a randomized, controlled animal study. Rats were anesthetized and the carotid artery was cannulated for mean arterial pressure and heart rate measurements while both jugular veins were cannulated for drug administration. All animals were infused with verapamil (15 mg/kg/h i.v.) until 45-60% reduction of mean arterial pressure and 30% reduction of heart rate were observed. After verapamil, control animals were given normal saline solution and the other groups received 4-aminopyridine (1 and 2 mg/kg/h) or Bay K 8644 (0.3 and 0.6 mg/kg/h) for 60 minutes. RESULTS: While 4-aminopyridine (1 mg/kg/h i.v.) did not significantly increase mean arterial pressure (75.9 +/- 5.5%) when compared with the control group (64.3 +/- 5.1%, p > 0.05), 2 mg/kg/h i.v. of 4-aminopyridine improved mean arterial pressure within 40 minutes (87.4 +/- 6.6%, p < 0.05, 95% CI 66.4-108.6%). Because the 2 mg/kg/h 4-aminopyridine produced side effects including seizures, secretions, and fasciculations at 35 +/- 5 minutes, the infusion was stopped at that time. Only the 2 mg/kg/h 4-aminopyridine infusion increased the heart rate at 10 and 20 minutes compared with the control group (p < 0.05, 95% CI 283.2-364.4). Bay K 8644 (0.3 and 0.6 mg/kg/h i.v.) significantly enhanced mean arterial pressure within 5 minutes (68.0 +/- 4.1% and 73.0 +/- 2.9%, respectively, p < 0.05), (95% CI 56.8-78.0% and 95% CI 64.9-81.1%, respectively) but no significant changes in mean arterial pressure were observed after 5 minutes. The 4-aminopyridine (2 mg/kg/h) increased the heart rate at 10 and 20 minutes compared with the control group (p < 0.05, 95% CI 311.3-358.7). Bay K 8644 did not produce a significant effect on heart rate (p > 0.05). CONCLUSIONS: 4-Aminopyridine improved mean arterial pressure and heart rate in a dose-dependent fashion; however, the higher infusion rate (2 mg/kg/h) necessary to improve mean arterial pressure and heart rate resulted in convulsions and excessive secretions. The reversal effects of Bay K 8644 on mean arterial pressure were transient and did not affect heart rate.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1997

The effects of amrinone and glucagon on verapamil-induced myocardial depression in a rat isolated heart model.

1. We measured the ability of glucagon and amrinone, used alone and in combination, to improve the myocardial function in a rat isolated heart model of calcium channel blocker (CCB) cardiotoxicity. 2. Verapamil 10(-4) mol consistently decreased heart rate and cardiac contractile force in our Langendorff rat isolated heart preparations. Glucagon increased the heart rate in a dose-dependent fashion. Amrinone increased the heart rate only at the 1 x 10(-1) mol concentration, and had no significant effect on cardiac contractility. 3. A positive linear correlation was found between the glucagon concentration and the percent recovery of baseline contractile force. 4. Although complete reversal of verapamil-induced myocardial depression occurred at glucagon concentrations of > 3 x 10(-6) mol, amrinone produced only 23.8 +/- 3.6% recovery from baseline at its highest concentration (4 x 10(-3) mol). 5. When glucagon and amrinone were administered together, there was no additional increase over glucagon alone in the increase in contractile force. 6. Glucagon, and not amrinone, is an appropriate agent, capable of reversing verapamil-induced myocardial toxicity in this rat isolated heart model. In vivo studies should be performed to assess whether this may be a reliable therapy in clinical cases.

Amrinone↗

PubMed1997

Relationship between high serum digoxin levels and toxicity.

A retrospective study of 1,269 patients on digoxin was done to determine the relationship between serum digoxin levels of 3.0 ng/ml or higher and clinical toxicity. Of 1,269 patients, 58 (4.6%) had digoxin serum levels of 3.0 ng/ml or higher. Clinical evidence of digoxin toxicity was present in only 11 of these patients and premature blood sampling accounted for the high levels in 10 other nontoxic patients. None of the patients with clinical toxicity died. The other 37 patients tolerated the high digoxin levels without exhibiting toxic effect. Low cardiac output, concomitant use of other drugs, and impaired renal function increased the serum digoxin levels in patients with and without clinical toxicity. Appropriate therapeutic digoxin level monitoring and confirmatory laboratory-clinical relationship may have important influences on these results. Additional work on further definition of "toxic" digoxin levels needs to be performed.

Adult↗

PubMed1996

The effects of amrinone and glucagon on verapamil-induced cardiovascular toxicity in anaesthetized rats.

The goal of this study was to compare the effects of glucagon and amrinone on mean arterial pressure (MAP) and heart rate, when used alone and in combination, in an anaesthetized rat model of verapamil toxicity. Rats were anaesthetized and the carotid artery was cannulated for MAP and heart rate measurements. Jugular and femoral veins were cannulated for drug administration. After verapamil infusion (15 mg/kg/h), control animals were given normal saline solution and the other groups received amrinone (0.1 or 0.2 mg/kg/min), glucagon (0.3 mg/kg bolus followed by 0.1 or 0.2 mg/ kg/min infusion), glucagon plus amrinone (0.1 mg/kg/min and 0.1 mg/kg/min respectively) or glucagon plus amrinone (0.2 mg/kg/min and 0.1 mg/kg/min respectively). Glucagon (0.2 mg/kg/min) significantly increased MAP when compared to the control group (P < 0.01). The combination of glucagon and amrinone did not produce a synergistic effect for the recovery of MAP. Furthermore, this combination masked the positive effects of glucagon (0.2 mg/kg/min) on MAP. Glucagon (0.2 mg/kg/min) increased the heart rates compared with those of the control group (P < 0.05). Additionally, amrinone (0.1 mg/kg/min) plus glucagon (0.1 mg/kg/min) increased the heart rates (P < 0.05). Finally, glucagon dose dependently recovered MAP. While amrinone depressed MAP in combination with glucagon, it did not alter the positive chronotropic effect of high dose glucagon.

Amrinone↗

PubMed1996

Multiple-dose activated charcoal in an accidental vancomycin overdose.

BACKGROUND: Multiple-dose activated charcoal may enhance the enterocapillary clearance of vancomycin. CASE REPORT: A 17-day-old female neonate born with congenital meningomyelocele and Arnold-Chiari malformation was iatrogenically overdosed with a 500 mg intravenous bolus of vancomycin during a shunt operation. The Red Man's Syndrome developed within minutes, characterized by sudden hypotension, skin rash and cyanosis. Serum vancomycin level at one hour after the injection was 165.7 micrograms/mL, as measured by an enzyme immunoassay method (EMIT). Multiple dose activated charcoal, 1 g/kg, was first given five hours after injection, and continued every four hours for 12 doses. The half-life of vancomycin during charcoal administration was calculated to be 9.4 h or less than the reported 13.4-33.7 h half-life in normal neonates. The neonate's renal function tests and brainstem auditory responses remained normal. CONCLUSIONS: Gastrointestinal dialysis with multiple-dose activated charcoal without cathartics appeared to shorten the elimination half-life of vancomycin.

Anti-Bacterial Agents↗

PubMed1995

Prevention of oral dichlorvos toxicity by different activated charcoal products in mice.

STUDY OBJECTIVE: To determine whether immediate treatment with oral activated charcoal (AC) products of differing surface areas prevents clinical toxicity of a lethal oral dose of dichlorvos in mice. DESIGN: An in vivo, prospective, randomized, placebo-controlled study using 75 male albino mice. INTERVENTIONS: Fasting mice were administered 57.5 mg/kg of a 0.55% dichlorvos solution via feeding tube. One minute later, groups of 15 mice each received 1 or 2 g/kg of Actidose-Aqua AC or 1 or 2 g/kg of Sigma AC or sterile water by feeding tube. In this way, all mice received 15 mL/kg of an AC suspension or sterile water. The animals were observed for 24 hours for seizures or death. RESULTS: In all treatment groups, mice were found to have significantly fewer seizures and deaths (P < .05) than the control group when compared by chi 2 and Fisher's exact tests. No statistical difference was found between the death and seizure rates when treatment groups were compared with each other. The group sizes were too small, however, to rule out significant type II error (beta > .2). CONCLUSION: In this in vivo mouse model, all AC products tested decreased the incidence of seizures and death. Further studies should be done to investigate the clinical effects of AC products with different surface areas.

Administration, Oral↗

PubMed1995

Urginea maritima (squill) toxicity.

A 55 year-old female ingested two bulbs of Urginea maritime (squill) plant as a folk remedy for her arthritic pains. Her past history was significant for Hashimoto thyroiditis and she was hypothyroid upon presentation. Subsequent effects resembling those seen with cardiac glycoside intoxication included nausea, vomiting, seizures, hyperkalemia, atrioventricular block and ventricular arrhythmias resembling digitalis toxicity. A serum digoxin level by an enzyme immunoassay method was 1.59 ng/mL. Despite supportive treatment and pacing, the patient expired from ventricular arrhythmias 30 h after ingestion. Squill has been recognized since antiquity for the clinical toxicity of its cardiac glycosides, but this appears to be the first report of a fatality since 1966.

Digoxin↗

PubMed1994

In vitro adsorption of dichlorvos and parathion by activated charcoal.

Accidental and suicidal ingestions of organophosphate compounds continue to be a common occurrence in Turkey. Activated charcoal administration without gastric emptying has been advocated as primary therapy in most acute poisoning cases, although some references do not recommend activated charcoal use in organophosphate poisoning. This study was performed to determine the in vitro adsorption of dimethyl dichlorovinyl phosphate (dichlorvos) and parathion by activated charcoal over a wide range of charcoal:organophosphate ratios (1:1, 2.5:1, 5:1, 10:1 and 20:1, g:g). The charcoal binding ability of dichlorvos and parathion were studied in both pH 1.2 and pH 7 environments. The supernatant was extracted with n-hexane and then analyzed by gas chromatography. Each incremental increase in charcoal dose increased the percent adsorption of dichlorvos and parathion. At the 20:1 ratio, 82.8 +/- 2.0/87.3 +/- 2.9% (pH 1.2/7.0) of dichlorvos and 59.3 +/- 4.5/64.5 +/- 6.1% (pH 1.2/7.0) of parathion were bound by activated charcoal. There were no significant differences in amounts of compound bound in the acid and neutral solutions. Large doses of activated charcoal effectively bind dichlorvos and parathion in vitro. In vivo research should be performed to determine activated charcoal's role in organophosphate poisoning cases.

Adsorption↗

PubMed1994

The effects of theophylline on serum alprazolam levels.

Theophylline and benzodiazepines are frequently combined in clinical practice. Because of a number of case reports about antagonism of benzodiazepine-induced sedation by theophylline, we investigated serum alprazolam levels in a convenient sample of pulmonary medicine inpatients receiving theophylline and no theophylline. One mg of alprazolam was given daily for seven days to 6 patients receiving theophylline and 7 patients not receiving theophylline treatment. On days 2 through 7, trough serum alprazolam levels were measured. On day 7, blood samples were collected before (0 hour), and at 3, 6, 9 and 12 hours after alprazolam administration. In patients receiving theophylline, serum trough alprazolam levels were significantly lower during each day of the study. In patients receiving no theophylline, serum alprazolam levels were in the therapeutic range, except for two patients who had high alprazolam levels. In this small study, serum alprazolam levels were found to be consistently below the therapeutic range in patients receiving chronic theophylline treatment. Previously reported antagonism of anxiolytic effects of benzodiazepines by theophylline is probably due to the lower serum benzodiazepine levels in these patients.

Adult↗

PubMed1994

Gentamicin excretion and uptake from breast milk by nursing infants.

OBJECTIVE: To investigate the excretion of gentamicin into human breast milk and resulting serum gentamicin levels in nursing newborn infants. METHODS: Women delivered by cesarean received gentamicin, 240 mg/day (80 mg intramuscularly three times a day) for 5 days postpartum. On day 4, maternal serum samples were collected 1 and 7 hours after gentamicin administration. Milk samples were collected 1, 3, 5, and 7 hours following administration. The infants were fed 1 hour after gentamicin administration, and serum samples were collected from the newborns 1 hour later. The concentrations of gentamicin were measured by a fluorescence polarization immunoassay. RESULTS: The mean (+/- standard deviation) maternal serum gentamicin levels at 1 and 7 hours were 3.94 +/- 1.12 and 1.02 +/- 0.78 microgram/mL, respectively. Milk gentamicin levels were: 0.42 +/- 0.26, 0.48 +/- 0.17, 0.49 +/- 0.17, and 0.41 +/- 0.25 microgram/mL at 1, 3, 5, and 7 hours, respectively. The mean milk:plasma gentamicin ratios were 0.11 and 0.44 at 1 and 7 hours, respectively. The correlation between maternal peak serum levels and milk levels was not statistically significant (P > .05). Detectable (above 0.27 microgram/mL) gentamicin levels were found in five of the ten newborn serum samples, with a mean level of 0.41 +/- 0.05 microgram/mL. CONCLUSION: Gentamicin is transferred into breast milk, and half of nursing newborn infants have detectable serum gentamicin levels.

Adult↗