Biomedical subjects

M Haburcák

Publications and source records attributed to M Haburcák.

8 recordsLinked to original sources

PubMed1998

Mannitol derivate used as a marker for voltammetrically monitored transport across the blood-brain barrier under condition of locus coeruleus stimulation.

1-Deoxy-1-nitro-D-mannitol (DN-Man) was used (femoral vein injection, approximate concentration in the blood 30 mmol.l-1) in pentobarbital anaesthetized rats as a promising marker detectable by differential pulse voltammetry (DPV) to study its transport across the blood-brain barrier (BBB) to the extra-cellular space of the frontoparietal cortex. DN-Man detection limit in in vitro calibrations (saline, blood) using DPV and carbon fiber microelectrodes was 0.5 mmol.l-1 with a good linearity (r = = 0.996) over the entire tested range (up to 30 mmol.l-1). The slow time-course of the rise of DN-Man signal (y = 106/(1 + (17.8/t)3)) in the cortex confirmed the functional BBB state. Electrical stimulation of the locus coeruleus (LC) (300 rectangular pulses at a frequency of 100 Hz, 1 mA, pulse duration 0.2 ms) elevated significantly DN-Man current in the cortex (to 168 +/- 59% of the control, mean +/- S.D., n = 8). The evoked permeation increase of the BBB to DN-Man was short-lasting (minutes), and the second LC stimulation (repeated 5 min after the first one) was ineffective. This fact was probably due to the reduction of DN-Man levels in blood and/or an altered response of microvessels to neurotransmitters. It was shown here that, under carefully controlled surgical and experimental conditions, DPV and DN-Man might be useful for the monitoring of the regional dynamics of BBB transport changes. The presented results also support the view that BBB transport can be influenced by LC neuronal activity.

Animals↗

PubMed1997

Calcium-activated potassium channels in cultured human endothelial cells are not directly modulated by nitric oxide.

Nitric oxide has been proposed to directly activated large conductance Ca(2+)-dependent K+ channels (BKCa) [Bolotina V.M., Najibi S., Palacino J.J., Pagano P.J., Cohen R.A. Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle. Nature 1994; 368: 850-853]. The nitric oxide (NO) donor S-nitrosocysteine (SNOC) was used to evaluate a possible direct modulation of BKCa by NO in EAhy926 (EA cells), a cultured human umbilical vein derived endothelial cell line, using the whole-cell, cell-attached and inside-out configuration of the patch-clamp technique, together with simultaneous amperometric measurement of NO and the concentration of free intracellular calcium [Ca2+]i. BKCa channels with a large conductance of approximately 190 pS, voltage-dependent activation and a reversal potential close to -80 mV have been identified in EA cells. Exposure of EA cells in the experimental chamber to 1 mM SNOC delivered approximately 5 microM NO, as recorded by an amperometric probe in situ. SNOC produced a modest increases in [Ca2+]i that was insufficient to activate BKCa channels. NO alone neither activated BKCa channels directly nor modulated preactivated BKCa channels in EA cells. These results do not support a direct modulatory effect of NO on large conductance BKCa channels in cultured endothelial cells.

Cells, Cultured↗

PubMed1996

Transport of an antihypoxic drug stobadine across the blood-brain barrier in rat striatum and its influence on catecholamine-oxidative current: a voltammetric study under normal and anoxic/ischaemic conditions.

Differential pulse voltammetry with a carbon fibre microelectrode (ME) was used in pentobarbital-anaesthetized rats for monitoring the stobadine current (STB.C) on both sides of the blood-brain barrier (BBB) in the arterial bloodstream (BS) and in the corpus striatum (CS). The STB.C exhibited a distinct peak at a polarization voltage 540 +/- 30 mV (n = 4). The maximum of STB.C in BS attained 2-3 min after the STB administration (2.8 mg/100 g in 1.0 ml saline solution i.a.) was followed by a rapid decrease to about 20% within next 3 min. The STB readily passed across the BBB: the STB.C peak appeared in the CS in the 3rd minute and continued to rise up to the 30th min. The administration of STB did not prevent a large increase (1347 +/- 326%, n = 3) of the catechol-oxidative current (CA.OC) occurring in the CS between the 4th and 5th minute after cardiac arrest. However, a decrease of ME sensitivity to CA.OC in the presence of STB was observed. This fact leads to the speculation whether a similar "quenching" of dopamine by STB could not participate in the protective effects of STB observed in the brain exposed to hypoxia-reoxygenation.

Animals↗

PubMed1994

Decrease of extracellular catecholamine content in the vicinity of cortical penicillin-induced epileptogenic focus: voltammetric study in the rat.

Differential pulse voltammetry with carbon-fibre microelectrodes was used in chloralhydrate-anaesthetized rats to test the influence of the penicillin-G-Na (PNC)-induced (topical application, approximately 2000 IU) epileptic activity on the catecholamine content (catechol-oxidative current, CA.OC) in the parietal cortex. In the experimental group (n = 4) after PNC a nonlinear CA.OC lowering was observed; this decrease during the first 10 min was faster than in the control group (n = 4). Significantly different values were observed from the 4th min after application. The best fit for this experimental curve gave the logarithmic function (f(t) = a+b.ln(t), a = 105.8, b = -10.6) with regression coefficient r = 0.98. From the 12th min after PNC application until the end of the experiments (54th min) CA.OC values ranged from 78% to 84% of the control group.

Anesthesia↗

PubMed1994

Catecholamine overflow within rat striatum: the influence of microstimulation and electroconvulsive stimulation as observed with voltammetry.

Differential pulse voltammetry with a carbon fibre microelectrode was used in chloral hydrate-anaesthetized rats for testing the influence of microstimulation and of electroconvulsive stimulation on the changes in concentration of electro-oxidizable materials (catechol derivates) in the extracellular space of the corpus striatum. Microstimulation applied in the striatum (8 V anodal pulses, 0.1 ms, 100 Hz for 40 s) caused a significant increase of the catechol-oxidative current (Ico); 5 s after microstimulation was stopped Ico ranged from 117 to 141% of the control (all values means +/- S.D. unless otherwise stated; 124 +/- 11%, n = 4, P < or = 0.01, Student's t test). This effect ceased in the third minute after microstimulation. A comparable result was observed when microstimulation was repeated at intervals of 10 min. Electroconvulsive stimulation with a sinusoidal current (50 Hz, approximately 150 mA, 0.2 s) caused a large increase in Ico; 20 s after stimulation ceased, Ico was 987 +/- 90% (n = 3) of the control and it returned to the baseline 2 min later. The mechanisms inducing transmitter overflow are considered and the influence of electroconvulsive stimulation on the striatum is discussed in the context of its beneficial effects in psychopathic patients.

Animals↗

PubMed1994

Effects of electroconvulsive shock on catecholamine release in the corpus striatum of the rat: a voltammetric study.

A voltammetric technique was used (differential pulse voltammetry with a carbon fibre microelectrode) to investigate dynamics of the changes of catecholamine overflow in the corpus striatum following electroconvulsive stimulation (ECS) of chloral hydrate-anaesthetized rats. Application of "maximal" ECS (50 Hz, AC, sine wave, approximately 150 mA, 0.2 s) caused large enhancement of catechol-oxidative current (CA.OC): In the first minute after its arrest, the CA.OC peak raised to 1032 +/- 405% (n = 5, mean +/- S.D.) of the controls (P < or = 0.001, Student's t-test). This large elevation of the extracellular catecholamine content ceased rapidly--the baseline level was attained in the second minute. CA.OC changes evoked by a "minimal" ECS (50 Hz, AC, sine wave, approximately 30 mA, 0.2 s) were equivocal in the first minute (increase, decrease: 145 +/- 56%, P > 0.05, n = 6). Possible mechanisms of the ECS therapeutic effect are discussed.

Animals↗

PubMed1993

Increase of catecholamine content in the extracellular space of the rat's brain cortex during spreading depression wave as determined by voltammetry.

The effect of chemically initiated (KCl) spreading cortical depression on catecholamine content in the extracellular cortical space was examined using voltammetry technique in chloralhydrate-anaesthetized rats. Correlation between alterations in catechol-oxidative current (CA.OC) and the time-course of the slow potential (SP) change (one of the chief features of the spreading depression) showed that spreading depression wave was accompanied by the significant increase in CA.OC content (up to 158 +/- 43%, mean +/- S.D., P < 0.001). The rise of the negative SP preceded significant CA.OC increase by 20 +/- 8 s. This fact provides the evidence that catecholamine overflow cannot participate in triggering spreading depression wave; nevertheless it can be an important link of the spreading depression mechanism.

Animals↗

PubMed1993

Clustering of cholesterol in DMPC bilayers as indicated by membrane mechanical properties.

Mechanical characteristics of bilayer lipid membranes (BLM) composed of dimyristoylphosphatidylcholine (DMPC) and cholesterol in the gel and liquid crystalline state were studied by measuring the modulus of elasticity in direction perpendicular to the BLM plane, E perpendicular. The value of E perpendicular varied nonmonotonically with the cholesterol concentration, with a maximum around c = 50 mol% cholesterol. E perpendicular of BLM in gel state was about 2 times higher than that measured for the liquid crystalline state but the shape of E perpendicular (c) curves was similar for both states of the membrane. This may be due to the formation of cholesterol clusters at c > 50 mol% in both phase states of BLM.

Cholesterol↗