High-performance liquid column and thin-layer chromatographic determination of human serum glibenclamide at therapeutic levels

Uihlein, M.; Sistovaris, N.

doi:10.1016/s0378-4347(00)80359-x

Cited by 36 publications

(12 citation statements)

References 8 publications

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“…The majority of the kinetic studies with oral glibenclamide have employed doses of up to 7.5 mg day-1 in either healthy humans or diabetic patients (Adams et al, 1982;Arnquist et al, 1983;Ayanoglu et al, 1983;McEwen, 1984;Matsuda et al, 1983;Prendergast, 1984;Sartor et al, 1980b;Uihlein & Sistovaris, 1982). Our present study using dosages up to 20 mg has thus yielded similar kinetic characteristics for glibenclamide to those reported by other investigators who have used drug specific analytical methods (Adams et al, 1982;Marchetti & Navalesi, 1989;Pearson et al, 1986).…”

Section: Discussionsupporting

confidence: 82%

Pharmacokinetic and pharmacodynamic studies of glibenclamide in non‐ insulin dependent diabetes mellitus.

Coppack

Lant

McIntosh

et al. 1990

Brit J Clinical Pharma

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1 The pharmacokinetic and pharmacodynamic properties of oral glibenclamide have been studied in 31 hospitalised in-patients and 79 ambulant out-patients with diabetes mellitus. 2 Breakfast was found to have no significant influence on the kinetic behaviour of glibenclamide or on the effect of this drug on blood glucose utilisation. 3 The time course of glibenclamide kinetics after 20 mg dosing was adequately described by a two-compartment open model, yielding mean half-lives of 3.3 ± 1.5 h (t½/,X) and 9.7 ± 1.2 (t½,z) for the initial and terminal elimination phases respectively. 4 No significant accumulation or change in kinetic profile occurred in patients who had normal renal and hepatic function, were treated continuously with glibenclamide, and then rechallenged after 8-12 weeks.5 Despite inter-individual variations in drug absorption, peak plasma concentrations (Cmax) and the area under the plasma concentration-time curve (AUC(0-24)) were dosedependent over the dose range 5-20 mg. No significant dose-response behaviour was observed in respect of glucose utilisation, suggesting that there is little clinical benefit in using doses of glibenclamide above 5 mg day-'. 6 Comparison of plasma glibenclamide concentrations at different time-bands following doses of 5 and 10 mg showed a wider range in ambulant out-patients than in age-, sexmatched in-patients treated with the same dosages of drug. Mean plasma drug concentrations attained at all time bands up to 8 h after dosing were higher in out-patients than in in-patients, suggesting a tendency to 'over-compliance' by patients in anticipation of attendance at clinic.

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Section: Discussionsupporting

confidence: 82%

Pharmacokinetic and pharmacodynamic studies of glibenclamide in non‐ insulin dependent diabetes mellitus.

Coppack

Lant

McIntosh

et al. 1990

Brit J Clinical Pharma

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“…In these serum samples drug concentrations were determined at the laboratories of Hoechst AG, Frankfurt, Germany. Glibenclamide was determined, using a validated specific radioimmunoassay (RIA) [23]. The detection limit was 1-3 ng/ml.…”

Section: Methodsmentioning

confidence: 99%

Blockade of vascular ATP-sensitive potassium channels reduces the vasodilator response to ischaemia in humans

et al. 1996

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In 1983, Noma [1] was the first to describe that an outward potassium current increased significantly when guinea pig or rabbit cardiac muscle cells were subjected to hypoxia. This current was caused by the activation of potassium channels, which was independent of the intracellular Ca 2+ concentration, but dependent on the intracellular concentration of adenosine-5 ′-triphosphate ([ATP] i ). These so-called ATPsensitive potassium (K ATP ) channels were suggested to play a cardioprotective role during ischaemia. Later, K ATP channels were also found in skeletal muscle [2], smooth muscle [3] and pancreatic beta cells [4] from animals. In pancreatic beta cells the K ATP channels mediate insulin secretion [5] and are a target for sulphonylurea derivatives in the treatment of non-insulin-dependent diabetes mellitus (NIDDM) [6]. Sulphonylurea derivatives are highly specific in blocking pancreatic and cardiovascular K ATP channels, and Diabetologia (1996Diabetologia ( ) 39: 1562Diabetologia ( -1568 Blockade of vascular ATP-sensitive potassium channels reduces the vasodilator response to ischaemia in humans Summary Experimental data show that ATP-sensitive potassium (K ATP ) channels not only occur in pancreatic beta cells, but also in the cardiovascular system, where they mediate important cardioprotective mechanisms. Sulphonylurea derivatives can block the cardiovascular K ATP channels and may therefore interfere with these cardioprotective mechanisms. Therefore, it is of clinical importance to investigate whether sulphonylurea derivatives interact with vascular K ATP channels in humans. Using venous-occlusion strain-gauge plethysmography, we investigated whether ischaemia-induced reactive hyperaemia is reduced by the sulphonylurea derivative glibenclamide in 12 healthy male non-smoking volunteers. Forearm vasodilator responses to three periods of arterial occlusion (2, 5 and 13 min) during concomitant infusion of placebo into the brachial artery were compared with responses during concomitant intra-arterial infusion of glibenclamide (0.33A control study (n = 6) showed that time itself did not change the vasodilator response to ischaemia.Glibenclamide significantly increased minimal vascular resistance (from 2.1 ± 0.1 to 2.3 ± 0.2 arbitrary units, Student's t-test: p = 0.01), and reduced mean forearm blood flow (from 37.5 ± 2.0 to 35.4 ± 2.0 ml ⋅ min -1 ⋅ dl -1 after 13 min occlusion, ANOVA with repeated measures: p = 0.006) and flow debt repayment during the first reperfusion minute (ANOVA with repeated measures: p = 0.04). In contrast, total flow debt repayment was not affected. Infusion of glibenclamide into the brachial artery resulted in local concentrations in the clinically relevant range, whereas the systemic concentration remained too low to elicit hypoglycaemic effects. Our results suggest that therapeutic concentrations of glibenclamide induce a slight but significant reduction in the early and peak vasodilation during reactive hyperaemia.

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“…The most commonly employed method for the analysis of glyburide is HPLC [4,5,6,8,9,14,15]. Different methods coupled with UV detection [9], fluorescence detection [5] or mass spectrometry [8] have been developed.…”

Section: Introductionmentioning

confidence: 99%

A simple and rapid HPLC method for the detection of glyburide in plasma original research communication (analytical)

Gedeon

Kapur

Aleksa

et al. 2008

Clinical Biochemistry

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High-performance liquid column and thin-layer chromatographic determination of human serum glibenclamide at therapeutic levels

Cited by 36 publications

References 8 publications

Pharmacokinetic and pharmacodynamic studies of glibenclamide in non‐ insulin dependent diabetes mellitus.

Pharmacokinetic and pharmacodynamic studies of glibenclamide in non‐ insulin dependent diabetes mellitus.

Blockade of vascular ATP-sensitive potassium channels reduces the vasodilator response to ischaemia in humans

A simple and rapid HPLC method for the detection of glyburide in plasma original research communication (analytical)

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