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
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9200210
Knihovny.cz E-resources
- MeSH
- Biological Transport MeSH
- Corpus Striatum metabolism MeSH
- Dopamine metabolism pharmacology MeSH
- Electrophysiology MeSH
- Blood-Brain Barrier physiology MeSH
- Brain Ischemia metabolism MeSH
- Carbolines blood pharmacokinetics pharmacology MeSH
- Catecholamines analysis metabolism MeSH
- Rats MeSH
- Microelectrodes MeSH
- Hypoxia, Brain metabolism MeSH
- Oxidation-Reduction MeSH
- Rats, Wistar MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- dicarbine MeSH Browser
- Dopamine MeSH
- Carbolines MeSH
- Catecholamines MeSH
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.