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1.
目的:探讨左乙拉西坦与苯巴比妥的药物相互作用及作用机制。方法:临床药师通过神经内科ICU的一例伴难以控制、反复发作癫的急性重症脑炎病例用药发现问题,查阅病历资料及相关文献进行分析。结果:左乙拉西坦可引起苯巴比妥血药浓度降低,可能与两者竞争结合P糖蛋白有关。结论:临床药师应该加强对左乙拉西坦的药物相互作用的观察和研究,以促进抗癫药物的合理应用。 相似文献
2.
Distinct differences have been described in the development of C3H/He mouse liver tumors induced by the genotoxic carcinogen diethylnitrosamine (DEN) and by the nongenotoxic agent phenobarbitone (PB) in terms of pathology and the frequency of mutation at codon 61 of the Ha-ras oncogene. To further define the mechanisms involved, we screened the tumor suppressor gene p53 for mutations in exons 5, 7, and 8 using polymerase chain reaction (PCR)–single-strand conformation polymorphism (SSCP) analysis. Nearly all the mutations so far described have been found within these three exons. In this study a total of six spontaneous tumors, eight tumors induced by PB, 14 tumors induced by DEN, and five samples of normal liver tissue were screened, and no mutations were found in any of the tumors examined. The positive control, the plasmid LTRp53cG (val), had a point mutation in exon 5 that was detected by PCR-SSCP. Since many of the tumors were late-stage hepatocellular carcinomas, we concluded that mutations in exons 5, 7, and 8 of the p53 gene do not play an important role in the development of chemically induced liver tumors in the C3H/He mouse. © 1994 Wiley-Liss, Inc. 相似文献
3.
BACKGROUND: Few reliable and reproducible animal models of acute hepatic failure exist or conform to the criteria proposed by Terblanche and Hickman (Dig. Dis. Sci. 36: 770, 1991). In this prospective randomized study we describe the selective induction of CYP450 enzymes, depletion of glutathione, and hepatotoxic insult using acetaminophen in the development and characterization of a novel rabbit model of acute hepatic failure. MATERIALS AND METHODS: Male New Zealand white rabbits weighing 3-5 kg were used. After preliminary dose ranging experiments, two groups of New Zealand white (n = 8 in each group) rabbits had CYP450 induction with phenobarbitone (40 mg/kg ip for 5 days) or with 20-methylcholanthrene (80 mg/kg ip). The glutathione synthetase inhibitor buthionine sulfoxime (2 mmol/kg iv) was then administered prior to acetaminophen administration (500 mg/kg sc). Clinical observations were recorded and arterial blood was sampled over 72 h. RESULTS: Grade I-III encephalopathy occurred at 5-12, 12-25, and 28-56 h, respectively, in animals pretreated with 20-methylcholanthrene, but not in the phenobarbitone pretreated group. Mortality was 75% in the 20-methylcholanthrene group compared to 0% in the phenobarbitone group. Blood lactate (P < 0.05), prothrombin time (P < 0.005), aspartate transaminase (P < 0.005), and creatinine (P < 0.05) were higher in the 20-methylcholanthrene group compared to the phenobarbitone group. Histological changes were marked in the 20-methylcholanthrene group with massive coagulative hepatic necrosis compared to minimal histological damage in the phenobarbitone group. CONCLUSION: The induction with 20-methylcholanthrene, glutathione depletion with buthionine sulfoxime, and subcutaneous administration of acetaminophen have led to the development of an animal model that parallels clinical, biochemical, and histological features of human hepatic failure. 相似文献
4.
G. W. Houghton A. Richens P. A. Toseland S. Davidson M. A. Falconer 《European journal of clinical pharmacology》1975,9(1):73-78
Summary Plasma, brain, lumbar CSF, skeletal muscle, skin and bone concentrations of phenytoin, phenobarbitone and primidone have been measured in specimens from patients undergoing temporal lobectomy for chronic epilepsy. A good correlation was found between the plasma and brain concentrations of each drug. Similarly, a good correlation was found between the plasma and CSF concentrations of each drug. Assuming that CSF is an ultrafiltrate of plasma, the percentage of phenytoin, phenobarbitone and primidone which was unbound in plasma was 10–14%, 43% and 81% respectively. Skeletal muscle concentrations of phenytoin and phenobarbitone and the skin concentration of phenytoin, also correlated with the plasma concentrations, but the remaining tissues did not give significant correlations. 相似文献
5.
A micromethod for estimating free levels of phenobarbitone, phenytoin and carbamazepine in patients' sera is described. Serum samples are subjected to a process of ultrafiltration, the filtrates treated with acetonitrile and the drug concentration quantified using high performance liquid chromatography. The stability of free levels in specimens before and after storage is investigated. The method is reproducible and mean recovery exceeds 98.5% showing that there is no significant absorption of drug onto the filters used. There is no interference from other substances normally present in patients' sera and there is a good correlation between results obtained by this method and a fluorescence polarisation immunoassay with correlation coefficient between 0.975 and 0.999. Serum samples can be stored for a lengthy period before ultrafiltration without adverse effects. The relevance of the method to patient care is discussed. 相似文献
6.
L. de Angelis 《Drug development research》1991,23(4):359-364
The potential anxiolytic effects of some calcium channel antagonists (nifedipine, nicardipine, and ±verapamil) were investigated in the elevated plus-maze test in mice. The acute effects of the above-mentioned drugs were compared with those of phenobarbitone and ±propanolol. Results showed that control mice spent less time in the open than in the closed arms, reflecting increased anxiety. Both phenobarbitone (20 mg/kg i.p.) and ±propanolol (5 mg/kg i.p.) increased the percentage of entries into open arms as well as the time spent on the open arms. Nifedipine (2 and 4 mg/kg i.p.), nicardipine (0.5 and 1.0 mg/kg i.p.), and ±verapamil (5 and 10 mg/kg i.p.) failed to alter significantly the behavior of mice. In summary, although there have been some reports based on other tests that calcium antagonists may have potential anxiolytic properties, this conclusion has not been supported by our results from the elevated plus-maze test. 相似文献
7.
Bertil Waldeck 《Basic & clinical pharmacology & toxicology》1975,36(2):172-180
Abstract: Mice were first given 10 mg/kg caffeine or saline, and 30 min. later pentobarbitone, 4 to 32 mg/kg. Both drugs caused an increased locomotor activity per se. However, when 16 mg/kg pentobarbitone was given after caffeine, the effects appeared to be more than additive. Similar results were obtained when phenobarbitone was substituted for pentobarbitone, and also when the order caffeine-phenobarbitone was reversed. In another experiment mice received reserpine, 10 mg/kg, 6 hrs before the combined treatment with ET495 and clonidine, which are known to stimulate central dopamine (DA) and noradrenaline (NA) receptors respectively. Caffeine, but not pentobarbitone, markedly enhanced the reversal of the reserpine-induced suppression of locomotor activity elicited by ET 495 + clonidine. Caffeine and pentobarbitone in combination were not more effective than caffeine alone in this respect. There were no obvious changes in the whole-brain levels of NA and DA after treatment with caffeine or pentobarbitone or both. However, when combined, the two drugs caused a decreased disappearance of DA following inhibition of tyrosine hydroxylase by α-methyl-p-tyrosine. It is suggested that central catecholamine mechanisms are involved in the interaction between caffeine and barbiturates. 相似文献
8.
Rats were fed either sodium phenobarbitone (PB) or betanaphthoflavone (BNF) for seven days. Deethylation of 7-ethoxyresorufin ( 7ERR ) and 7-ethoxycoumarin ( 7EC ) was measured in small and large intestine and liver, and cytochrome P-450 in liver. Our semi-purified diet was shown to produce minimal levels of intestinal deethylation activity. BNF was added to the semi purified diet and fed at levels from 0.1 to 100 mg BNF/kg of diet. Significant (P less than 0.05) induction of deethylation in small intestine was seen at all dose levels, ranging from 2-fold at 0.1 mg/kg diet to greater than 100-fold at 100 mg/kg diet. A 3-fold increase was also seen in the large intestine at 50 mg/kg. A significant increase in hepatic deethylation was only seen at 100 mg/kg. PB was administered in drinking water at 50, 100 and 1000 mg PB/l. Significant (P less than 0.05) induction of hepatic deethylation was seen at all dose levels, ranging from 2-fold at 50 mg/l to 5-fold at 1000 mg/l. Hepatic cytochrome P450 was also increased. No significant increase in intestinal deethylation was seen at any of the doses used. 相似文献
9.
The microsomal monooxygenase system of adult rat hepatocytes in short-term non-proliferating culture could be induced by phenobarbitone and benzanthracene. Differences in the kinetics of induction and the additive nature of the inductions indicated that induction by the two agents occurred by different mechanisms and the use of haemoprotein-selective inhibitors demonstrated the induction of different haemoproteins by the two agents. The type of haemoprotein present in the cells altered during a four day culture period. 相似文献
10.
S. N. WICKRAMASINGHE JUDITH SAUNDERS GAIL WILLIAMS 《European journal of haematology》1976,17(4):312-316
Suspensions of human bone marrow cells were incubated with various concentrations of phenobarbitone or phenytoin sodium for 2 h, and the effects of this incubation on the subsequent incorporation of 3H-thymidine and 3H-leucine into DNA and protein, respectively, were studied. Both drugs caused a depression of 3H-thymidine incorporation and this phenomenon was not prevented by the addition of 100 μg of pteroylglutamic acid, folinic acid or 5-methyltetrahydrofolate per ml of marrow culture. The lowest concentration of drug which caused a statistically significant depression of 3H-thymidine incorporation was 200 μg per ml for phenobarbitone and 50 μg per ml for phenytoin sodium. Both phenobarbitone and phenytoin sodium also caused an increase in the incorporation of 3H-leucine at concentrations of 50 and 20 μg per ml, respectively, suggesting the possibility that a stimulation of protein synthesis within erythropoietic cells may play an important role in the development of anticonvulsant-induced macrocytosis. 相似文献