PubMed · 7309254
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T H Corbett. 1981. Carcinogenesis.. https://doi.org/10.1097/00004311-198119040-00008
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The simultaneous enantioseparation of selected anesthetic drugs was studied by capillary electrophoresis (CE) in presence of three different negatively charged cyclodextrins (CDs). Among the chiral selectors tested, namely carboxymethyl, sulfobutyl ether and sulfated-beta-CD, the latter appeared to be the most effective to achieve the enantiomeric resolution of the investigated compounds. Beside CD type, resolution was greatly influenced by the buffer pH, the molecular structure of the anesthetic compounds, CD concentration and temperature. The optimum electrophoretic conditions for the stereoselective analysis of the studied anesthetics were obtained with a poly(vinyl alcohol) coated capillary (48.5 cm total length x 50 microm I.D.), a 50 mM Tris-phosphate buffer at pH 2.5 containing 6 mg ml(-1) of sulfated-beta-CD, an applied voltage of 30 kV and a temperature of 30 degrees C. Under these optimized conditions, four drugs, namely bupivacaine, mepivacaine, ketamine and prilocaine, were simultaneously enantioresolved in less than 12 min. Furthermore, the method was applied to the stereoselective analysis of mepivacaine in a pharmaceutical preparation. Finally, the method was on-line coupled to electrospray ionization mass spectrometry using the counter current partial-filling technique.
Cortical spreading depression (CSD) may be the underlying mechanism of migraine aura. The role of CSD in initiating a migraine headache remains to be determined, but it might involve specific changes in gene expression in the brain. To examine these changes, four episodes of CSD at 5-minute intervals were induced in the mouse brain by application of 300mM KCl, and gene expression was examined 2 hours later using cDNA array and reverse transcriptase-polymerase chain reaction. Controls consisted of groups that received anesthesia only, attachment of recording electrodes only, and application of 0.9% NaCl. Of the over 1,180 genes examined in our experiments, those consistently regulated by CSD included vasoactive peptides; the vasodilator atrial natriuretic peptide was induced by CSD, while the vasoconstrictor neuropeptide Y was downregulated. Other genes specifically regulated by CSD were involved in oxidative stress responses (major prion protein, glutathione-S-transferase-5, and apolipoprotein E). L-type calcium channel mRNA was upregulated. In summary, CSD regulates genes that are intrinsic to its propagation, that identify accompanying vascular responses as a potential source of pain, and that protect against its potential pathological consequences. We believe these observations have strong relevance to the mechanisms of migraine and its outcomes.
PURPOSE: To review recent findings concerning Ca(2+) channel subtype/structure/function from electrophysiological and molecular biological studies and to explain Ca(2+) channel diseases and the actions of anesthetics on Ca(2+) channels. SOURCE: The information was obtained from articles published recently and from our published work. PRINCIPAL FINDINGS: Voltage-dependent Ca(2+) channels serve as one of the important mechanisms for Ca(2+) influx into the cells, enabling the regulation of intracellular concentration of free Ca(2+). Recent advances both in electrophysiology and in molecular biology have made it possible to observe channel activity directly and to investigate channel functions at molecular levels. The Ca(2+) channel can be divided into subtypes according to electrophysiological characteristics, and each subtype has its own gene. The L-type Ca(2+) channel is the target of a large number of clinically important drugs, especially dihydropyridines, and binding sites of Ca(2+) antagonists have been clarified. The effects of various kinds of anesthetics in a variety of cell types have been demonstrated, and some clinical effects of anesthetics can be explained by the effects on Ca(2+) channels. It has recently become apparent that some hereditary diseases such as hypokalemic periodic paralysis result from calcium channelopathies. CONCLUSION: Recent advances both in electrophysiology and in molecular biology have made it possible to clarify the Ca(2+) channel structures, functions, genes, and the anesthetic actions on the channels in detail. The effects of anesthetics on the Ca(2+) channels either of patients with hereditary channelopathies or using gene mutation techniques are left to be discovered.