ISSN:0031-7012    

DOI:10.1159/000138512

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

We have demonstrated significant differences in 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization values between lymphocyte membranes of untreated rheumatoid arthritis patients and lymphocyte membranes of patients treated with antirheumatic drugs, such as hydroxychloroquine and auranofin. No difference has been detected in rheumatoid arthritis patients treated with auranofin associated with 6-methylprednisolone. The results indicate that some drugs used in the treatment of rheumatoid arthritis induce changes of lymphocyte membrane fluidity. The positive correlations between fluorescence polarization values and objective indices of the disease activity, as erythrocyte sedimentation rate, C-reactive protein, fibrinogen level, and α2-globulin, suggested that fluorescence polarization could be used in the study of the pharmacological action of antirheumatic drugs and in monitoring antirheumatic therapy

ISSN:0031-7012    

DOI:10.1159/000138513

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The role of adenosine 3’,5’-monophosphate (cAMP) in histamine-mediated vasomotion of coronary vascular smooth muscle was studied in the isolated perfused rabbit heart. In paired physiological studies, histamine-mediated vasoconstriction, as indicated by change in perfusion pressure, was inhibited by the presence of either theophylline, a phosphodiesterase inhibitor, or forskolin, an adenylate cyclase activator. The inhibitory effect of theophylline, but not of forskolin, was removed with cimetidine (H2-receptor antagonist). In biochemical studies, coronary vessel cAMP was measured immediately after, and compared to, the vasomotor response to histamine alone and to histamine in the presence of forskolin, theophylline, diphenhydramine (H1-receptor antagonist) or cimetidine. These studies showed that cAMP levels correlate inversely with the vasoconstrictor response to histamine, indicating that stimulation of H2-receptors is associated with a reduction of cAMP and that H2-receptors modify this reduct

ISSN:0031-7012    

DOI:10.1159/000138514

出版商:S. Karger AG    

年代:1989

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000138515

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Phenylephrine tested on the isolated endothelium intact rat aortic strips elicited an enhanced response in the second assay when compared with the response obtained in the first trial. Removal of the endothelium and the pretreatment of the strips in the endothelium with methylene blue almost completely prevented the enhanced response to phenylephrine in the second assay. Pretreatment of the strips with lysine acetyl salicylate failed to abolish the potentiated response to phenylephrine in the second test. These data were taken as an evidence that the basal production or release of endothelium-derived relaxing factor(s) but not cyclooxygenase products of arachidonic acid from the endothelium of the rat aorta can influence the contractile effect of phenylephrine and the enhanced response to this α-adrenoceptor agonist in the second assay is probably due to the recuded production or release of these endogenously occurring endothelium-originated substance(s)

ISSN:0031-7012    

DOI:10.1159/000138516

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Electrophysiological effects of ketanserin on pacemaker activity of rabbit sinus node cells were studied using double-microelectrode voltage clamp method. Ketanserin (10–5 mol/l) caused an increase in spontaneous cycle length accompanied by decreases in the maximum upstroke velocity of the action potential, the slope of the phase 4 depolarization and the action potential amplitude. On the current systems, ketanserin reduced the slow inward current (Isi) and the time-dependent potassium outward current (Iκ) in a dose-dependent manner. As for a decrease in the outward current, the agent did not change the steady-state activation of IK. These observations indicate that ketanserin does not have a specific effect on a single current system, but that the drug exerts an inhibitory effect on the electrical activity of the sinus node pacemaker cel

ISSN:0031-7012    

DOI:10.1159/000138517

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Anesthetized rats, maintained on an intravenous (1 ml/h) infusion of saline, were injected with either atrial extract from normal rats (AE), atriopeptin III (APIII, 24 amino acids) or atrial peptide (AP, 28 amino acids) as either a bolus injection (1 atrial equivalent of AE, 1 μg APIII, or 1 μg AP) or by constant infusion (1.7 ng APIII or AP/min for 30 min) in isotonic saline. Diuretic, natriuretic, and kaliuretic responses were determined by subtraction of baseline values from the renal response during the first 15 min after administration of the atrial natriuretic factor (ANF). The change in renal response observed in rats receiving saline and a bolus injection of an ANF was compared to the change in response observed in the same rats that received the dopaminergic antagonist, domperidone (0.2 μg/kg, i.v.), and the same ANF. In the case of the renal response following infusion of an ANF, a paired comparison was made between domperidone-treated and untreated rats. Domperidone attenuated the renal response to AP, administered either as a bolus injection or a constant infusion, whereas domperidone significantly reduced renal response to APIII only following constant infusion. The renal response to a bolus injection of AE was not affected by the administration of domperidone. These findings suggest that the renal action of the putative circulating form of ANF, i.e. AP, is mediated via dopaminergic receptors, and that the route of administration may affect the mechanism of action of an A

ISSN:0031-7012    

DOI:10.1159/000138518

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The role of glutathione status in gastric mucosal cytoprotection has been a subject of controversy. Cysteamine, an exogenous sulfhydryl agent and diethyl maleate (DEM), an endogenous glutathione (GSH) depletor both appear to protect rats from ethanol-induced gastric lesions. In this study, we used various agents to alter gastric mucosal GSH levels and assessed the effects on susceptibility to ethanol injury. We found that DEM and buthionine sulfoximine both depleted gastric GSH but only DEM protected against ethanol-induced gastric lesions. L-Oxothiazolidine-4-carboxylate (OXT) and N-acetyl-L-cysteine (NAC) both potentiated ethanol-induced gastric lesions even though only NAC significantly raised the GSH level. The depletion of GSH by DEM was reversed by supplying cysteine in the form of OXT or NAC so that the net result was a GSH level close to normal control. The potentiation of ethanol injury by NAC and OXT was still apparent. These experiments show no relation between gastric GSH levels and susceptibility to ethanol injury.

ISSN:0031-7012    

DOI:10.1159/000138519

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The elimination kinetics of probenecid in the rat was studied by using an in vitro liver perfusion system to estimate its basic elimination and in vivo to estimate its renal excretion by catheterization of the urinary bladder. In the liver perfusion study different amounts of probenecid were added to the perfusion medium yielding different initial concentrations (40, 200 and 400 μg/ml), and 4 different intravenous bolus doses (50, 75, 100 and 200 mg/kg) were administered in vivo to rats in order to evaluate the renal excretion. The results obtained were described by one-compartment models, with Michaelis-Menten elimination by the liver Vm = 67.4 ± 14.0 (SD) μg/min and a slightly decreasing Km with increasing initial concentrations [from 76.5 ± 9.0 to 53.2 ± (SD) 18.4 μg/ml]. The excretion by the kidney was characterized by a saturable pathway in parallel with first-order elimination, the maximum rate of the active transports Tm = 0.04 ± (SD) 0.09 μg/min, Km,r =100.3 ± (SD) 12.3 μg/ml and a linear renal clearance of 0.0008 ± (SD) 0.0

ISSN:0031-7012    

DOI:10.1159/000138520

出版商:S. Karger AG    

年代:1989

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000138521

出版商:S. Karger AG    

年代:1989

数据来源: Karger