Lower limb haemodynamics during antihypertensive treatment with metoprolol and propranolol.
Four polyvinyl chloride (PVC) matrix membrane electrodes responsive to 2 drugs affecting the urogenital system--oxybutynin hydrochloride (OX) and flavoxate hydrochloride (FX)--were developed, described, and characterized. A precipitation-based technique with tungstophosphate (TP) and ammonium reineckate (R) anions as electroactive materials in a PVC matrix with an OX cation was used for electrode 1 and 2 fabrication, respectively. Electrode 3 and 4 fabrication was based on use of the precipitation technique of FX cation with tetrakis (4-chlorophenyl) borate and R anions as electroactive materials. Fast and stable Nernstian responses in the range 1 x 10(-2)-1 x 10(-6) M for the 2 drugs over the pH range 5-8 revealed the performance characteristics of these electrodes, which were evaluated according to International Union of Pure and Applied Chemistry recommendations. The method was applied to FX and OX in their pharmaceutical formulations and in human plasma samples. The 4 proposed sensors were found to be specific for the drugs in the presence of up to 60% of their degradation products. Validation of the method according to the quality assurance standards showed suitability of the proposed electrodes for use in the quality control assessment of these drugs. The recoveries for determination of the drugs by the 4 proposed selective electrodes were 99.5 +/- 0.5, 100.0 +/- 0.4, 99.9 +/- 0.4, and 100.1 +/- 0.4% for sensors 1-4, respectively. Statistical comparison between the results obtained by this method and the official method of the drugs was done, and no significant difference found.
Flavoxate, a smooth muscle relaxant, compared with propantheline showed no significant difference in clinical effect on voiding disturbances in hyperactive neurogenic bladders, but fewer side effects. Both drugs increased bladder capacity significantly, but flavoxate did not increase residual urine in contrast to propantheline.
To assist the clinician in making informed decisions regarding UI, provide information on the wider ramifications of the disease, and provide a comprehensive overview of the condition.
Staurosporine as a protein kinases inhibitor induced cell death or neurite outgrowth in PC12 cells. We investigated the involvement of calcium channel and plasma membrane receptors on staurosporine inducing neurite outgrowth in PC12 cells. PC12 cells were preincubated with NMDA receptor inhibitors (1.8 mM ketamine and 1µM MK801, treatment 1) or L-Type Calcium channels (100 μM nifedipine and 100 µM flavoxate hydrochloride, treatment 2) or calcium-calmoduline kinasses (10 μM trifluoprazine, treatment 3) and nifedipine, MK801, flavoxate hydrochloride and ketamine (treatment4) or without pretreatments (control). Then, the cells were cultured in RPMI culture medium containing 214nM staurosporine for induction of neurite outgrowth. The percentage of Cell cytotoxicity and apoptotic index was assessed. Total neurite length (TNL) and fraction of cell differentiation were assessed. After 24h, the percentage of cell cytotoxicity were increased in treatments 1, 2 and 4 compared with control (p<0.05). After 6h, apoptotic index was similar between all treatments. After 12h, apoptotic index were increased in treatment 4 compared with control (p<0.05). After 24h, apoptotic index were increased in treatments 1, 2 and 4 compared with control (p<0.05). TNL were decreased in treatments 1, 2 and 4 compared with control in different times of assessment (6, 12 and 24 h) (p<0.05). The fraction of cell differentiation were decreased in treatments 1, 2 and 4 compared with control (p<0.05). It can be concluded that the possible involvement of L-type calcium channel and the N-methyl D-aspartate receptor on staurosporine-induced neurite outgrowth process in PC12 cells.
Retrospective analysis of data of participants in community, hospital or nursing home setting.
The effects of tiropramide on the isolated detrusor and intravesical pressure of the bladder in situ in rats were compared with those of flavoxate, oxybutynin and terodiline. The IC50 values (x 10(-5) M) of tiropramide for carbachol (CCh)-, K+ (60 mM)-, Ba2+ (10 mM)-, and electrical stimulation-induced contractions were 3.6, 4.2, 5.8, and 2.9, respectively. The four antispasmodics used (2 and 4 mg/kg, i.v., each) abolished the rhythmic bladder contractions in situ in anesthesized rats. Of the four compounds, oxybutynin was most potent and no significant differences were observed between the inhibitory effects of tiropramide, flavoxate and terodiline. The administration of flavoxate (30 and 60 mg/kg) into the duodenum little influenced the rhythmic bladder contractions. Tiropramide, flavoxate, oxybutynin and terodiline (8 and 12 mg/kg, i.v., each) dose-dependently prolonged the time to the volume-evoked micturition reflex, and the activity of tiropramide was not statistically different from those of the other three antispasmodics. Under unilateral pelvic and bilateral hypogastric nerve transection, both of the contractions induced by electrical stimulation of the peripheral and central cut ends of the pelvic nerve were dose-dependently inhibited to the same extent by tiropramide and terodiline. These results suggest that the effects of tiropramide on the function of urinary bladder in rats may be mainly due to direct actions on the smooth muscle, and that tiropramide is more potent than flavoxate and less potent than oxybutynin and terodiline.