Drugs online research references
Pol Arch Med Wewn. 1993 Jun;89(6):463-79.
[Alcohol tolerance in patients with non-insulin-dependent diabetes (type 2) treated orally with drugs--derivatives of sulphonylurea]
[Article in Polish]
Lao B, Czyzyk A, Szutowski M, Szczepanik Z.
Kliniki Gastroenterologii i Chorob Przemiany Materii, Warszawie.
The oral ethanol loading test (0.5 g per kg b.m. given as 40% solution) was carried out in 5 groups, each of 10 patients with non-insulin-dependent (type 2) diabetes before and after 10 days of treatment with one of the following sulphonylurea derivatives: tolbutamide 0.5 t.i.d., chlorpropamide 0.5 once daily morning, glibornuride 0.025 t.i.d, glibenclamide 0.005 t.i.d. and glipizide 0.005 t.i.d. The response to alcohol (facial flush, heart rate, blood pressure) were compared, and blood concentration of ethanol, acetaldehyde, pyruvate, lactate, carbonates as well as blood pH, pO2 and pCO2 were determined in fasting state and during 6 hours after alcohol ingestion. In all patients the family history of diabetes and the presence and degree of vascular complications were registered. Evident flushing phenomenon was observed in 6 patients treated with chlorpropamide, in 3 treated with tolbutamide, in 2 treated with glibenclamide, in one receiving glibornuride and in none treated with glipizide. All drugs caused a greater rise of blood ethanol and acetaldehyde levels in relation to the control tests, but the difference reached statistical significance only in the group receiving chlorpropamide. Moreover, patients (pooled) with positive thermographic response had also significantly higher blood levels of ethanol and acetaldehyde during the second test. The ratio of acetaldehyde to ethanol concentration in blood (mumol:mmol) was not significantly changed in any group indicating parallel impairment of both steps of ethanol metabolism. All studied drugs intensified to a similar degree the alcohol-induced hypoglycaemia, but had no significant effect on the decrease of blood pyruvate level neither on the increase of blood lactate level. They didn't change the post-alcohol decrease of blood bicarbonate and pH, and didn't modify the behaviour of partial gas pressure. There was also no difference between pooled groups of patients with positive and negative thermographic reaction with respect to family history of diabetes and frequency and intensity of vascular complications. It is concluded that in patients with non-insulin-dependent (type 2) diabetes the second generation sulphonylurea derivatives are associated with lower risk of alcohol intolerance in case of its incidental ingestion in small amounts. The hypothesis of association of positive thermographic reaction to alcohol during treatment with sulphonylurea derivatives with more frequent occurrence of diabetes in family members and lower tendency to vascular complications was not confirmed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8415209&dopt=Abstract
Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9431-5.
K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.
Heurteaux C, Bertaina V, Widmann C, Lazdunski M.
Institut de Pharmacologie Moleculaire et Cellulaire, Valbonne, France.
Transient global forebrain ischemia induces in rat brain a large increase of expression of the immediate early genes c-fos and c-jun and of the mRNAs for the 70-kDa heat-shock protein and for the form of the amyloid beta-protein precursor including the Kunitz-type protease-inhibitor domain. At 24 hr after ischemia, this increased expression is particularly observed in regions that are vulnerable to the deleterious effects of ischemia, such as pyramidal cells of the CA1 field in the hippocampus. In an attempt to find conditions which prevent the deleterious effects of ischemia, representatives of three different classes of K+ channel openers, (-)-cromakalim, nicorandil, and pinacidil, were administered both before ischemia and during the reperfusion period. This treatment totally blocked the ischemia-induced expression of the different genes. In addition it markedly protected neuronal cells against degeneration. The mechanism of the neuroprotective effects involves the opening of ATP-sensitive K+ channels since glipizide, a specific blocker of that type of channel, abolished the beneficial effects of K+ channel openers. The various classes of K+ channel openers seem to deserve attention as potential drugs for cerebral ischemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8415718&dopt=Abstract
Eur J Pharmacol. 1993 Jan 12;230(2):203-7.
ATP-dependent K+ channel blockers antagonize morphine- but not U-504,88H-induced antinociception.
Ocana M, Del Pozo E, Baeyens JM.
Department of Pharmacology, School of Medicine, University of Granada, Spain.
The effects of four ATP-dependent K+ channel blockers (hypoglycemic sulfonylureas) against morphine- and U50488H-induced antinociception were evaluated using the tail flick test in mice. None of the sulfonylureas tested significantly modified tail flick latency in control animals. However, i.c.v. pretreatment with gliquidone (0.4-1.6 micrograms/mouse), glipizide (2.5-10 micrograms/mouse), glibenclamide (10-40 micrograms/mouse) or tolbutamide (20-80 micrograms/mouse) dose dependently antagonized morphine-induced antinociception approximately equieffectively, the only difference being in potency: gliquidone > glipizide > glibenclamide > tolbutamide. This effect of sulfonylureas was very specific, since none antagonized the antinociception elicited by U50488H even at doses twice as great as the dose that induced maximum antagonism of morphine antinociception. Because morphine, but not U50488H, opens K+ channels in neurons and because the order of potency of the different sulfonylureas for blocking ATP-dependent K+ channels in neurons and for antagonizing morphine antinociception is the same, we suggest that morphine antinociception is mediated by the opening of ATP-dependent K+ channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8422902&dopt=Abstract
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