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31.
S. H. Sindrup L. Arendt-Nielsen K. Brøsen P. Bjerring H. R. Angelo B. Eriksen L. F. Gram 《European journal of clinical pharmacology》1992,42(6):587-591
Summary We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg). The study was performed in 16 extensive metabolizers of sparteine, using a double-blind, randomized, four-way, cross-over design. The treatments given at 3 h intervals during the four sessions were placebo/placebo, quinidine/placebo, placebo/codeine, and quinidine/codeine. We measured pin-prick pain and pain tolerance thresholds to high energy argon laser stimuli before and 1, 2, and 3 h after codeine or placebo.After codeine and placebo, the peak plasma concentration of morphine was 6–62 (median 18) nmol·.l–1. When quinidine pre-treatment was given, no morphine could be detected (<4 nmol·l–1) after codeine. The pin-prick pain thresholds were significantly increased after placebo/codeine, but not after quinidine/codeine compared with placebo/placebo. Both placebo/codeine and quinidine/codeine increased pain tolerance thresholds significantly. Quinidine/codeine and quinidine/placebo did not differ significantly for either pin-prick or tolerance pain thresholds.These results are compatible with local CYP2D6 mediated formation of morphine in the brain, not being blocked by quinidine. Alternatively, a hypoalgesic effect of quinidine might have confounded the results. 相似文献
32.
33.
Cyclosporine Interacts with Mycophenolic Acid by Inhibiting the Multidrug Resistance-Associated Protein 2 总被引:5,自引:0,他引:5
Dennis A. Hesselink Reinier M. van Hest Ron A. A. Mathot Fred Bonthuis Willem Weimar Ron W. F. de Bruin Teun van Gelder 《American journal of transplantation》2005,5(5):987-994
In mycophenolate mofetil (MMF)-treated organ transplant recipients, lower mycophenolic acid (MPA) plasma concentrations have been found in cyclosporine (CsA) compared with tacrolimus (Tac)-based immunosuppressive regimens. We previously demonstrated that CsA decreases exposure to MPA and increases exposure to its metabolite MPA-glucuronide (MPAG), possibly by interfering with the biliary excretion of MPAG. To elucidate the role of the multidrug resistance-associated protein (Mrp)-2 in the interaction between MMF and CsA, we treated three groups of 10 Mrp2-deficient rats (TR- rat) for 6 days with either vehicle, CsA (8 mg/kg) or Tac (4 mg/kg) by oral gavage. Hereafter, co-administration with MMF (20 mg/kg) was started in all groups and continued through day 14. The 24-h MPA/MPAG area under the concentration-time curve (AUC) was determined after single (day 7) and multiple MMF doses (day 14). On both study days, there were no significant differences in the mean MPA and MPAG AUC between CsA and Tac-treated animals. We conclude that the pharmacokinetics of MMF are comparable in Mrp2-deficient rats receiving either CsA or Tac as co-medication. This finding suggests that CsA-mediated inhibition of the biliary excretion of MPAG by the Mrp2 transporter is the mechanism responsible for the interaction between CsA and MMF. 相似文献
34.
Li‐Hsuan Wang Kuang‐Yang Hsu Yow‐Shieng Uang Feng‐Lin Hsu Li‐Ming Yang Shwu‐Jiuan Lin 《Phytotherapy research : PTR》2010,24(6):852-858
The impacts of caffeic acid (3,4‐dihydroxycinnamic acid, CA) on the pharmacokinetics of levodopa (L‐dopa) were studied in rabbits. A single dose of 5/1.25 mg·kg?1 l ‐dopa/carbidopa was administered alone or was co‐administered with three different doses of caffeic acid (2.5, 5, and 10 mg·kg?1), or a single dose of 5 mg·kg?1 caffeic acid was administered alone via an intramuscular route to six rabbits each in a crossover treatment protocol. Plasma levels of l ‐dopa, 3‐O‐methyldopa (3‐OMD), caffeic acid, and ferulic acid were determined and subsequently used to calculate their pharmacokinetic parameters. The results indicated that caffeic acid administered at a dose of 10 mg·kg?1 decreased about 22% of the peripheral formation of 3‐OMD and about 31% of the Cmax of 3‐OMD. In addition, the metabolic ratios (MR, AUC of 3‐OMD/AUC of L‐dopa) decreased by about 22%. Results also indicated that caffeic acid significantly decreased the proportion of 3‐OMD (p < 0.05). In contrast, the parameters of neither caffeic acid nor ferulic acid were significantly affected by l ‐dopa/carbidopa. In conclusion, caffeic acid at a dose of 10 mg·kg?1 can significantly affect the COMT metabolic pathway of L‐dopa. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献
35.
H. Davidowa D. Albrecht H.-J. Gabriel S. Heublein K. Wetzel 《The European journal of neuroscience》1995,7(12):2364-2369
The effect of iontophoretically applied cholecystokinin (CCK) on neurons of the neostriatum was studied in rats anaesthetized with urethane. The most frequently observed effect of the sulphated octapeptide (CCK-8S) on striatal neurons was excitation. Spontaneously active neurons responded more often to CCK-8S than quiescent cells. Silent, primarily non-responsive neurons could often be stimulated with CCK-8S using glutamate to induce an ongoing discharge. Thus, 45.8% of the 177 neurons studied changed their discharge rate by more than 30%. Certain CCK receptor antagonists could prevent the effect of CCK-8S, fully or at least partly, in the majority of CCK-responsive neurons. The data suggest that cholecystokinin modulates the firing of active neostriatal neurons via the CCKA or the CCKB receptor type. Furthermore, we compared neuronal responses to glutamate with those recorded during concomitant administration of CCK-8S in order to study the interaction of both transmitters, which may be colocalized in striatal afferents. CCK-8S mainly enhanced the excitatory effect of glutamate on striatal neurons, but in several neurons the response to glutamate was reduced. The CCKB receptor antagonist could prevent CCK-8S from increasing the glutamate-induced activation. 相似文献
36.
A. J. Pijl K. A. Solen† S. F. Mohammad R. Monson† L. S. Yu J. M. T. van Griensven D. B. Olsen W. J. Kolff 《Artificial organs》1990,14(2):125-129
Device-induced thrombogenesis was studied in an in vitro model using human blood circulated through an artificial ventricle. A new constant pressure filtration technique was used to detect circulating microemboli, the activated partial thromboplastin time (APTT) test was used to monitor the blood for the presence of anticoagulant activity of heparin, and hemolysis was quantified by measuring the plasma free hemoglobin level. Circulation of blood through a 20-ml stroke volume pneumatically driven ventricle for 6-9 h resulted in a significant reduction of APTT, indicating the loss of the anticoagulant effect of heparin. Microemboli concentration was minimal until the APTT decreased below 125 s, at which time the microemboli concentration increased rapidly. This was presumed to be due to the formation of thrombi following a decrease in heparin activity. A significant increase in hemolysis was also noted when blood was pumped. None of these changes was noted in the nonpumped control blood. Spontaneous loss of heparin activity in blood circulated by a pneumatically driven pump may have clinical implications and may help understanding of the problems associated with device-induced thrombogenesis. 相似文献
37.
对71例肾移植术后患者进行了氨苄青霉素与环孢菌素的相互作用研究。患者在开始服用氨苄青霉素之前、之中、之后的肾功能以及环孢菌素全血浓度测定结果表明,三项指标均无显著改变。另一组肾移植术后患者37例进行的诺氟沙星与环孢菌素相互作用研究,结果与氨苄青霉素的相互作用类似。提示氨苄青霉素、诺氟沙星可安全地与环孢菌素合用,而不影响肾功能。 相似文献
38.
39.
Jesus Galvez Lourdes Cabrera Francisco Lajarin Pilar Garcia-Pearrubia 《Journal of immunological methods》1994,170(2):197-210
New methods for simplified quantitation of effector-target conjugation have been developed. The binding unit (BU) is defined as the number of target cells required to bind a specified percentage of effector cells. The number of binding units is determined from binding isotherms in which effector conjugate frequencies are measured by holding constant the number of effector cells and by varying the number of target cells. Alternately, a binding unit can be defined as the number of effector cells required to bind a specified percentage of target cells. In this case, BU is computed from binding isotherms in which target conjugate frequencies are measured at different values of effector cells by holding constant the number of target cells. Also, the area under the curve (AUI) of these isotherms is another index that can be used as an overall measure of the binding capacity in an effector-target system. The experimental values of BU and AUI determined from effector and target isotherms agree well with theoretical predictions based on our previously developed binding model (J. Immunol. Methods (1992) 155, 133–147). The relationship between BU and AUI, and procedures to determine these parameters are shown. The value of these indices to express effector-target conjugation quantitatively has been confirmed by determining the values of BU and AUI for the NK-K562 effector-target system. 相似文献
40.
A. Tchelet T. Vogel D. Helman R. Guy C. Neospouolus V. Goffin J. Djiane A. Gertler 《Molecular and cellular endocrinology》1997,130(1-2):141-152
A new analogue of recombinant human growth hormone (hGH), hGH des(1–6,14) was expressed in Escherichia coli, refolded and purified to homogeneity. The mutation decreased the hormone's ability to bind lactogenic and somatogenic receptors through its site 1, and almost completely abolished its ability to bind these receptors through site 2, as evidenced by both binding and gel-filtration experiments. More specifically, the binding to prolactin receptors (PRLRs) from various species or their soluble recombinant extracellular domains (ECDs) was decreased 1.5–4-fold, whereas the binding to hGH receptor (hGHR) was decreased 10–85-fold. These changes caused an almost total loss of hormone agonistic activity in several in vitro bioassays and subsequently, the hGH des(1–6,14) analogue acquired antagonistic properties. This antagonistic activity was dependent upon modification of site 1. In those cases in which the binding was reduced only slightly, e.g. binding to rabbit PRLRs, hGH des(1–6,14) acted as a strong antagonist, whereas in others in which the binding of site 1 was reduced to a higher degree, such as other PRLRs and, in particular, hGHR, the antagonistic activity was correspondingly weaker. Circular dichroism spectra of the analogue suggested that these changes do not result from a decrease in overall -helix content, but rather from minor local structural modifications at the N-terminus. 相似文献