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At least 1,225 records · Page 68Linked to original sources
PubMed1999

[Prospects for future development in the pharmacology of gastric ulcer models and of gastric acid secretion in experimental animals].

Prospects for future development in the field of gastrointestinal pharmacology were briefly discussed on the base of the present progress in our own research on animal models of gastric ulcer and the mechanism of gastric acid secretion. We established a few novel methods to induce extensive ulceration restricted to the gastric antral area in rats by a combination of drug-induced vagal stimulation with necrotizing agents or anti-inflammatory drugs, as well as with ammonia in relation to the etiological role of Helicobacter pilori. In these models, it was found that the gastric antral area become sensitive to mucosal aggression under vagal stimulation and refeeding after starvation and that the mucosal primary afferent nervous system was involved in the integration of gastric mucosal defense mechanisms. Among many experimental gastric ulcer models, the gastric antral ulcer is important for future study because of its unique analogy with human ulcer in its location of incidence and pathology. We also established methods to measure gastric acid secretion in the isolated gastric mucosa or whole stomach of rat or mouse, as well as acid secretion in anesthetized rats. By using these methods, the signal transduction route of vagus nerve stimulation to parietal cells was studied. The importance of mediation of enterochromaffin cells in gastric acid secretion was clearly confirmed. In the studies on receptor mechanisms in the central nervous system regulating gastric acid secretion, critical roles of GABA, barbiturate, glutamate, neurosteroids and opioid receptors were clarified. From these results, several remaining problems were suggested and these must be resolved in future research.

Animals↗
PubMed1986

A trial of discontinuation of barbiturates in patients with secondary generalized epilepsy.

The vast majority of patients with secondary generalized epilepsy (SGE) were under polytherapy including barbiturates. We were able to completely withdraw barbiturates in 17 cases with a refractory course of SGE. Valproic acid (VPA) is considered as one of the best drugs for SGE. Barbiturates decrease the serum level of VPA and this may lead to a reduced efficacy of VPA. The dosage of VPA was adjusted to attain the level of 100-150 micrograms/ml. Barbiturates were then gradually decreased and finally discontinued. After six months of follow-up, 13 patients (76%) showed a reduced seizure frequency. Also, the physical and psychological conditions improved in a good number of cases. Barbiturates are not necessarily required in pharmacotherapy of SGE and may be safely withdrawn.

Adolescent↗
PubMed1976

A modified ultraviolet spectrophotometric method for the determination of theophylline in serum in the presence of barbiturates.

Ultraviolet spectrophotometry is the most commonly used technique for the determination of theophylline levels for therapeutic monitoring. Common interferences in most methods are barbiturates and xanthines. A modified method which eliminates interferences from barbiturates and most xanthines is presented. Theophylline is extracted from serum with chloroform/isopropanol at pH 7.4 back extracted into dilute hydrochloric acid and then the solution is made alkaline with sodium hydroxide. Barbiturate interferences are eliminated. Interference from caffeine, uric acid, 7-(2,3-dihydroxypropyl)theophylline, xanthine, and hypoxanthine are not observed. Theobromine, and the metabolite 3-methylxanthine interfere. Interference is not observed from quinidine, diazepam, salicylate, glutethimide, methylprylon, propranolol, methaqualone, dilatin and ethchlorvynol. Sulfanilamide, procainamide and chlordiazepoxide interfere.

Barbiturates↗
PubMed1993

Neurochemical actions of inhalational anesthetics at the GABAA receptor complex.

Pharmacologically relevant concentrations of inhalational anesthetics such as halothane, enflurane and isoflurane enhance [3H]flunitrazepam (FLU) binding to benzodiazepine receptors prepared from well-washed membranes of murine cerebral cortex and cerebellum. These effects were concentration dependent and markedly enhanced by addition of chloride to the incubation medium. Using halothane as a prototype inhalational agent, it was observed that like barbiturates, increases in [3H]FLU binding were effected through an increase apparent in the apparent affinity of this radioligand with no accompanying change in the maximum number of binding sites. Although previous reports have demonstrated barbiturates augment gamma-aminobutyric acid-enhanced [3H]benzodiazepine binding, halothane exerts an additive effect in the nominal absence of chloride. Isoflurane produces a significant reduction in the EC50 of pentobarbital-augmented [3H]FLU binding. Halothane modestly reduced the binding of a benzodiazepine receptor inverse agonist, [3H]Ro 15-4513. Significant differences were also observed in the potencies and efficacies of both isoflurane and enflurane to enhance [3H]FLU binding to benzodiazepine receptors in cerebellar and cortical membranes. These findings provide a possible molecular basis for the clinical observation that benzodiazepines and barbiturates augment the anesthetic properties of inhalational agents. Moreover, the regional differences in anesthetic potency and efficacy reported here suggest a differential interaction of these inhalational agents among gamma-aminobutyric acidA receptor isoforms.

Administration, Inhalation↗
PubMed1993

Acute, chronic and differential effects of several anesthetic barbiturates on glutamate receptor activation in neuronal culture.

The acute and chronic effects of several anesthetic barbiturates, in therapeutic concentrations, on the excitatory amino acid (EAA)-induced elevation of intracellular calcium levels ([Ca2+]i) were examined in neuronal tissue culture. The ultrashort-acting barbiturate, thiamylal, was effective in blocking elevations of [Ca2+]i induced by kainate, N-methyl-D-aspartate (NMDA), and quisqualate or by membrane depolarization with 40 mM KCl. The structurally similar barbiturate, secobarbital which differs from thiamylal only by having an oxygen in place of a sulfur, was able to block elevations induced by the above EAAs but was less effective than thiamylal and did not significantly reduce [Ca2+]i that resulted from membrane depolarization with KCl. Pentobarbital, while differing from secobarbital by only a methyl group, was without effect on either the NMDA- or 40 mM KCl-induced elevations of [Ca2+]i. By contrast, cyproheptadine, a compound that has been shown to block Ca2+ channels, has a different profile from the above barbiturates in that cyproheptadine is more effective in blocking elevation of [Ca2+]i induced by membrane depolarization with KCl while the barbiturates are more effective in reducing [Ca2+]i induced by EAAs. An anticonvulsant barbiturate, phenobarbital, did not reduced elevations of [Ca2+]i induced by any EAA tested or by membrane depolarization with KCl. When cells were treated chronically with thiamylal for 4 days, 2-6 h after the abrupt drug withdrawal there was a hyperresponsiveness to the elevations of [Ca2+]i induced by both kainate and NMDA but not by quisqualate. A similar hyperresponsiveness was not seen after the chronic treatment with phenobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of hCGRP I and II on gastric blood flow and acid secretion in anesthetized rabbits.

Effects of intravenously administered human calcitonin gene-related peptides (hCGRP) I and II on regional blood flow and gastric acid secretion were examined in barbiturate-anesthetized rabbits. Blood flow was measured by injection of radioactively labeled microspheres at 0, 10, 20, 30, and 60 min. hCGRP I and II and vehicle were infused intravenously in five rabbits in rising doses of 0.01 (0-10th min), 0.03 (11-20th min), and 0.1 microgram.kg-1.min-1 (21-30th min). hCGRP I and II increased gastric blood flow dose dependently. Moreover, hCGRP I raised regional conductance (inverse of vascular resistance) in the stomach, duodenum, heart, brain, and skeletal muscle. As a result of the increased total peripheral conductance the mean arterial pressure was reduced, but the cardiac output remained unchanged. hCGRP II increased blood flow and conductance selectively in the stomach and the pancreas. The total peripheral conductance and mean arterial pressure remained unchanged. Apparently, hCGRP II exerts a more localized effect on the stomach than hCGRP I. hCGRP I and II did not affect basal gastric acid secretion. Pentagastrin-stimulated acid secretion was increased by 28% with hCGRP I (0.025 micrograms.kg-1.min-1) and decreased by 27% with hCGRP II (0.025 micrograms.kg-1.min-1). The inverse effect of hCGRP I and II and the parallel stimulation of blood flow brought about with hCGRP I and II indicate a different mode of action of the peptides on gastric blood flow and gastric acid secretion.

Animals↗
PubMed1992

Mechanisms of neurotransmission of valproate sodium in suppressing barbiturate and phenytoin withdrawal syndrome.

The present study was undertaken to investigate some important processes of neurotransmission which occur in rat brains under the influence of valproate sodium. Valproate sodium is used for the suppression of the withdrawal effects resulting from sudden discontinuation of phenobarbital and phenytoin treatment. Corpus striatum, hippocampus and cortex were isolated operatively. The amounts of neuromediators (dopamine, noradrenaline, serotonin and gamma-aminobutyric acid) were determined using fluorometry. The results show that the anti-withdrawal effect of valproate sodium established in previous research probably is due to active metabolites which increase the amount of gamma-aminobutyric acid in all brain structures. In suppressing barbiturate and phenytoin withdrawal syndrome using valproate sodium, the previously established anti-withdrawal effect probably is due to high tissue levels of dopamine in hippocampus and to noradrenaline in the cortex, hippocampus and corpus striatum. This anti-withdrawal effect continues for three days after the discontinuation of valproate sodium. This probably is due to the accumulation of the inhibitory neuromediator GABA in the cortex, hippocampus and corpus striatum and to the elevated level of dopamine in hippocampus. The results raise new possibilities for developing medicinal substances, which possess anti-withdrawal action, from the metabolites of the valproate sodium.

Animals↗