Biomedical subjects

S Kalkan

Publications and source records attributed to S Kalkan.

13 recordsLinked to original sources

PubMed2007

Vasorelaxant effect of iloprost on isolated human internal mammary artery.

In this study, vasodilator effect of iloprost on KCl-induced contraction in human internal mammary artery (IMA) was studied and compared with other vasodilators papaverin and diltiazem. Ring segments of IMA were studied in organ baths for measurement of isometric tension. After the tissues has reached their baseline tension, precontraction was induced by 100 mm KCl and cumulative concentration-relaxation was measured by the application of iloprost (10(-9)-10(-6) m), papaverine (10(-5)-10(-4) m), diltiazem (10(-9)-10(-4) m) or ethanol; a solvent for iloprost; alone. The maximal relaxation of IMA segments to iloprost was 13.5 +/- 2.2%. Iloprost caused significantly limited relaxation when compared with papaverin (106.0 +/- 2.9%) and diltiazem (93.6 +/- 2.5%) (P < 0.001). Papaverin produced the greatest maximal relaxation to KCl-induced contraction of IMA. The potency of iloprost (-log EC(50) = 6.59 +/- 0.19) was significantly higher than those of papaverine (-log EC(50) = 4.21 +/- 0.11) and diltiazem (-log EC(50) = 5.63 +/- 0.06) (P < 0.001). In addition, -log EC(50) of diltiazem was significantly greater than papaverin (P < 0.001). Iloprost appears to be more potent than those of papaverine and diltiazem but it was inefficient in maximal inhibition on KCl-induced contraction. Iloprost may have little benefit in KCl-related vasoconstriction on human IMA segments.

Adult↗

PubMed2006

Interrelation between the Poisoning Severity Score, carboxyhaemoglobin levels and in-hospital clinical course of carbon monoxide poisoning.

The aim of the present study is to evaluate the relationship between the Poisoning Severity Score (PSS) and carboxyhaemoglobin (COHb) levels in patients with carbon monoxide poisoning (COP) using outcome as the measure. The study was designed as a retrospective chart review of patients with final diagnosis of COP. Correlation of PSS and COHb levels at presentation was evaluated with collected data. Majority of the cases were grade 1 (minor) PSS (134 cases, 73.6%) and 93.4% of these patients made a complete recovery. There were six deaths (mortality 3.3%) and six in-hospital major complications (IHMCs) (3.3%) (please specify whether the complications were in the patients who died). There is moderate correlation between PSS and outcome (p < 0.001, r = 0.493). Grade 3 (severe) PSS was significantly different from other grades for outcome (six mortalities and three IHMCs). Patients classified as grade 3 and patients who died had a significantly higher mean age (p < 0.05, 41.8 +/- 23.6 and p < 0.01, 60.1 +/- 20.3, respectively). Mean COHb level of grade 3 (33.2 +/- 13.9%) was significantly higher than that of other grades (p < 0.05). COHb levels according to outcome were not different (? within the patients in grade 3). Decreased level of consciousness, acidosis, tachycardia, high glucose and leucocyte levels showed significant relation with higher PSS, COHb level and adverse outcome. We conclude that the PSS is a reliable guide in COP. Value of the PSS in COP may be enhanced if additional factors and investigations are included.

Adult↗

PubMed2005

Local image structures and optic flow estimation.

Different kinds of local image structures (such as homogeneous, edge-like and junction-like patches) can be distinguished by the intrinsic dimensionality of the local signals. Intrinsic dimensionality makes use of variance from a point and a line in spectral representation of the signal in order to classify it as homogeneous, edge-like or junction-like. The concept of intrinsic dimensionality has been mostly exercised using discrete formulations; however, recent work has introduced a continuous definition. The current study analyzes the distribution of local patches in natural images according to this continuous understanding of intrinsic dimensionality. This distribution reveals specific patterns than can be also associated to local image structures established in computer vision and which can be related to orientation and optic flow features. In particular, we link quantitative and qualitative properties of optic-flow error estimates to these patterns. In this way, we also introduce a new tool for better analysis of optic flow algorithms.

Algorithms↗

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↗

PubMed2003

Diffusion-weighted MR imaging of pleural fluid: differentiation of transudative vs exudative pleural effusions.

The aim of this study was to evaluate the ability of diffusion-weighted MRI in differentiating transudative from exudative pleural effusions. Fifty-seven patients with pleural effusion were studied. Diffusion-weighted imaging (DWI) was performed with an echo-planar imaging (EPI) sequence (b values 0, 1000 s/mm(2)) in 52 patients. The apparent diffusion coefficient (ADC) values were reconstructed from three different regions. Subsequently, thoracentesis was performed and the pleural fluid was analyzed. Laboratory results revealed 20 transudative and 32 exudative effusions. Transudates had a mean ADC value of 3.42+/-0.76 x 10(-3) mm(2)/s. Exudates had a mean ADC value of 3.18+/-1.82 x 10(-3) mm(2)/s. The optimum cutoff point for ADC values was 3.38 x 10(-3) mm(2)/s with a sensitivity of 90.6% and specificity of 85%. A significant negative correlation was seen between ADC values and pleural fluid protein, albumin concentrations and lactate dehydrogenase (LDH) measurements ( r=-0.69, -0.66, and -0.46, respectively; p<0.01). The positive predictive value, negative predictive value, and diagnostic accuracy of ADC values were determined to be 90.6, 85, and 88.5%, respectively. The application of diffusion gradients to analyze pleural fluid may be an alternative to the thoracentesis. Non-invasive characterization of a pleural effusion by means of DWI with single-shot EPI technique may obviate the need for thoracentesis with its associated patient morbidity.

Diagnosis, Differential↗

PubMed2001

Effects of subchronic parathion exposure on cyclosporine pharmacokinetics in rats.

Parathion undergoes enzymatic oxidation by hepatic cytochrome P-450 (CYP450) enzymes to the active metabolite paraoxon. Consequently, alterations in CYP450-dependent oxidation may affect the pharmacokinetics and pharmacodynamics of drugs that are metabolized in the liver. The CYP3A family is known to be responsible for the majority of cyclosporine metabolism. The aim of the present study was to assess the disposition kinetics of cyclosporine during subchronic parathion exposure. Male Wistar rats were administered either water or two different doses of parathion (1/100 LD50, 1/25 LD50; LD50 = 14 mg/kg) by gavage for 6 wk. Subsequently, rats in each experimental group received a single oral dose of cyclosporine (10 mg/kg), and serial blood samples were drawn from the carotid artery over a period of 48 h. Pharmacokinetic analysis showed that parathion increased the blood cyclosporine concentration twofold as evidenced by AUC (area under the curve), half life (t 1/2) and peak plasma concentration (Cmax). This may be due to inhibition of cyclosporine metabolism, an interaction that may be of clinical relevance in immunosuppression therapy.

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↗

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

Effect of verapamil on responses to endothelin-1 in aortic rings from streptozotocin-induced diabetic rats.

In this study, we investigated the constrictor responsiveness to endothelin-1 (ET-1, 10-30 n m) of aortic rings (under 1 g resting tension in Krebs-Bicarbonate solution) from 8-weeks streptozotocin (STZ, 65 mg kg-1, i.p)-induced diabetic rats and vehicle-treated control rats. The maximum ET-1-induced contraction of the aorta in diabetic rats was increased by 150%, but the EC50 of ET-1 remained unchanged. Although in both groups, verapamil reduced the constrictor responses to ET-1 (diabetic group P<0.001, control group P<0.05), there were not any significant differences between PD2 values. These results suggest that verapamil inhibits ET-1-induced Ca2+ entry through the L-type channel and this effect did not change in diabetes mellitus.

Animals↗

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

The effect of acute bilateral adrenalectomy on serotonin-induced inhibition of gastric acid secretion and acute gastric mucosal injury in rats.

Serotonin (5-hydroxytryptamine, 5-HT) produces many changes in gastric functional parameters, including the inhibition of gastric acid secretion and changes in mucosal blood flow. Exogenous 5-HT has also been shown to induce gastric erosion. The influence of adrenalectomy on experimental lesions in the rat gastric mucosa remains controversial. The aim of this study was to see the effects of adrenalectomy on pentagastrin stimulated gastric acid secretion in anaesthetized male Wistar rats. Gastric acid was collected via cannulae placed in the stomach. 5-HT (3.5 mumol/kg, i.v.) inhibited pentagastrin stimulated acid output by 54% and produced haemorrhagic gastric lesions with a mean ulcer index of 2 +/- 0.3. Adrenalectomy prevented both 5-HT induced inhibition of gastric acid secretion and mucosal injury. The results suggest that the effects of 5-HT require an intact adrenal gland.

Adrenal Glands↗