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At least 685 records · Page 38Linked to original sources
PubMed1990

A double-blind study of the efficacy of topical ketorolac tromethamine gel in the treatment of ankle sprain, in comparison to placebo and etofenamate.

In a double-blind, placebo-controlled study the efficacy and safety of topical ketorolac tromethamine were assessed in the reduction of inflammation and pain due to ankle sprain. Ketorolac 2% gel was compared with etofenamate and placebo (ketorolac vehicle) in a 15-day study. Patients attended for visits on days 1 (admission), 2, 3, 4, 8, and 15 of the study. Measurements of efficacy were ankle volume, pain measured on visual analogue scales (VAS) and verbal rating of pain. Safety was assessed by volunteered adverse events and vital signs. A total of 37 patients was admitted to the study of whom 13 received ketorolac, 12 placebo, and 12 etofenamate. One patient receiving ketorolac was lost to follow-up on day 15 owing to an unrelated accident. The remaining 36 patients completed the study. Ketorolac was significantly better than placebo in reducing the volume of the injured ankle based on the maximum, the area under the curve, and the day 15 percentage changes in ankle volume. Results for etofenamate were similar to those for ketorolac for all three variables and there were no significant differences between the active treatments. Reductions in VAS pain at rest were more marked in the ketorolac group than either of the other groups at all visits. On day 4 the differences between ketorolac and each of the other groups were statistically significant. Reductions in VAS pain on movement were also greatest for the ketorolac group at all visits. The differences between ketorolac and each of the other groups achieved statistical significance on days 4 and 8, but were marginal in terms of significance on day 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1994

Synthesis of the cholesteryl ester prodrugs cholesteryl ibuprofen and cholesteryl flufenamate and their formulation into phospholipid microemulsions.

Phospholipid micoremulsions have been suggested as a drug-delivery system for hydrophobic compounds. In this study hydrophobicity was achieved by derivatizing with cholesterol. Cholesteryl ibuprofen (3) and cholesteryl flufenamate (4) were synthesized. 3 was isolated as an amorphous, white solid with a melting range of 114-120 degrees C. 4 was isolated as a crystalline, white solid with a melting range of 145-148 degrees C. The proposed structures of 3 and 4 were supported by IR, NMR, MS, and organic microanalysis. Phospholipid:cholesteryl ester microemulsions were prepared by the addition of a 1-propanol solution of the cholesteryl ester, other lipids, and phospholipid to a rapidly mixing KCl/KBr solution. The hydrophobic phase was modified by the addition of cholesteryl oleate or triolein to study the effect of the fluidity of the hydrophobic core on the formation of the microemulsions. The results indicated that a molar ratio of 75:25 and a total lipid concentration of 60 mg/mL consistently gave microemulsions with a mean size of 100-150 nm. In addition, the formation of eutectic mixtures of 3 and 4 with cholesteryl oleate were determined to be 16% (w/w) for 3 and 12% (w/w) for 4; melting points were 35.2 and 45.2 degrees C, respectively. The solubilities of 3 and 4 in triolein were determined to be 13.2% (w/w) and 11.5% (w/w), respectively. Other investigators have shown that if the core of a phospholipid:cholesteryl estermicroemulsion exists in a liquid state at physiologic temperature, the turnover of the cholesteryl esters from these microemulsions occurs at a faster rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Availability↗
PubMed2001

Effects of some pharmacological agents on the survival of unipedicled venous flaps: an experimental study.

Clinical and experimental studies have been conducted to improve the survival of venous flaps. As a result of these studies, although various survival mechanisms were raised, none obtained satisfactory information. Venous stasis, and the resultant venous thrombosis, is a factor that decreases the survival of venous flaps. In this study, we evaluated the effects of two antiinflammatory agents, etodolac and etofenamate, on the survival of unipedicled venous flaps. In this study, 35 male New Zealand white rabbits (3,500-4,000 g) (70 ears) were used. Perichondrocutaneous flaps, 3 x 4.5 cm in size, were designed and raised, keeping the central veins intact in the middle of venous flap. Central arteries and nerves were ligated and transected both proximally and distally, to prepare unipedicled venous flaps. A silicone sheet was placed between the cartilage tissue and flap, to prevent blood flow and revascularization beneath. The subjects were divided into seven groups, consisting of five rabbits (10 ears). In the negative control group (group I), the single vascular pedicle of venous flaps, central veins were ligated and flaps sutured into their own place as the composite graft. In the positive control group (group II), after venous flaps were prepared, normal saline, 0.2 mL, was given subcutaneously. In the first of five experimental groups (group III), unfractionated heparin (100 U/day) was given subcutaneously. In the second experimental group (group IV), etodolac (5 mg/kg/day) was given subcutaneously. In the third experimental group (group V), etophenamate (5 mg/kg/day) was given orally through a feeding tube. In the fourth experimental group (group VI), parnaparin (5 anti-Xa U/kg/day) was given subcutaneously. In the fifth experimental group (group VII), nadroparin (5 anti-Xa U/kg/day) was given subcutaneously, about 7 days postoperatively. At the eighth postoperative day, surviving areas of venous flaps were measured, and the results were evaluated by Kruskal-Wallis ANOVA and Mann-Whitney U-test (P < 0.05). Biopsies were also taken from the flaps for histological evaluation of border of necrotic tissue. Surviving areas of unipedicled venous flaps were larger in experimental groups than those in negative and positive control group (P < 0.05). However, comparison of the experimental groups demonstrated no statistically significant difference (P > 0.05). We concluded that all pharmacological agents used in the experimental groups succeeded in increasing the survival of unipedicled venous flaps. Survival of the unipedicled venous flap was higher in venous flaps than that of composite graft, clearly showing the importance of the venous pedicle.

Animals↗
PubMed1994

Flufenamate and Gd3+ inhibit stimulated Ca2+ influx in the epithelial cell line CFPAC-1.

The relevant influx pathway for stimulated Ca2+ entry into epithelial cells is largely unknown. Using flufenamate (Flu) and Gd3+, both known pharmacological blockers of non-selective cation currents in other epithelial preparations, we tested whether the stimulated Ca2+ entry in CFPAC-1 cells was inhibited by these agents. Transmembraneous Ca2+ influx into CFPAC-1 cells was stimulated by either ATP (10(-4) and 10(-5) mol/l), carbachol (CCH, 10(-4) mol/l) or thapsigargin (TG, 10(-8) mol/l). Three different experimental approaches were used. (1) Because the plateau phase of an agonist-induced [Ca2+]i transient reflects Ca2+ influx into these cells, we investigated the influence of Flu and Gd3+ on the level of the stimulated [Ca2+]i plateau. (2) The fura-2 Mn(2+)-quenching technique was used to visualise divalent cation entry and monitor its inhibition. (3) During the "refilling period" after agonist-induced discharge of the intracellular pools the putative influx inhibitors Flu and Gd3+ were given and subsequently the filling state of the agonist-sensitive intracellular stores tested. The results from the first experimental approach showed that both Flu and Gd3+ were potent inhibitors of the stimulated Ca2+ entry in CFPAC-1 cells. Flu reversibly decreased the ATP-induced [Ca2+]i plateau in a concentration dependent manner, with an IC50 value of 33 mumol/l (n = 6). Similar results were obtained for the CCH- (n = 5) and the TG-induced (n = 5) [Ca2+]i plateau. Gd3+ concentration dependently inhibited the stimulated Ca2+ plateau. A complete block of the ATP-induced [Ca2+]i plateau was seen at 0.5 mumol/l (ATP 10(-5) mol/l, n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed2001

Calcium-sensitive nonselective cation channel identified in the epithelial cells isolated from the endolymphatic sac of guinea pigs.

We identified a Ca2+-sensitive cation channel in acutely dissociated epithelial cells from the endolymphatic sac (ES) of guinea pigs using the patch-clamp technique. Single-channel recordings showed that the cation channel had a conductance of 24.0 +/- 1.3 pS (n = 8) in our standard solution. The relative ionic permeability of the channel was in the order K+ = Na+ > Ca2+ >> Cl-. This channel was weakly voltage-dependent but was strongly activated by Ca2+ on the cytosolic side at a concentration of around 1 mm in inside-out excised patches. With cell-attached patches, however, the channel was activated by much lower Ca2+ concentrations. Treatment of the cells, under cell-attached configuration, with ionomycin (10 microm), carbonyl cyanide 3-chlorophenylhydrazone (CCCP, 20 microm), or ATP (1 mm), which increased intracellular Ca2+ concentration ([Ca2+]i), activated the channel at an estimated [Ca2+]i from 0.6 microm to 10 microm. It is suggested that some activators of the channel were deteriorated or washed out during the formation of excised patches. Based on this Ca2+ sensitivity, we speculated that the channel contributes to the regulation of ionic balance and volume of the ES by absorbing Na+ under certain pathological conditions that will increase [Ca2+]i. This is the first report of single-channel recordings in endolymphatic sac epithelial cells.

Adenosine Triphosphate↗
PubMed1998

Apical Cl- channels in A6 cells.

Short-circuit current (Isc), transepithelial conductance (Gt), electrical capacitance (CT) and the fluctuation in Isc were analyzed in polarized epithelial cells from the distal nephron of Xenopus laevis (A6 cell line). Tissues were incubated with Na+- and Cl--free solutions on the apical surface. Basolateral perfusate was NaCl-Ringer. Agents that increase cellular cAMP evoked increases in Gt, CT, Isc and generated a Lorentzian Isc-noise. The responses could be related to active, electrogenic secretion of Cl-. Arginine-vasotocin and oxytocin caused a typical peak-plateau response pattern. Stimulation with a membrane-permeant nonhydrolyzable cAMP analogue or forskolin showed stable increases in Gt with only moderate peaking of Isc. Phosphodiesterase inhibitors also stimulated Cl- secretion with peaking responses in Gt and Isc. All stimulants elicited a spontaneous Lorentzian noise, originating from the activated apical Cl- channel, with almost identical corner frequency (40-50 Hz). Repetitive challenge with the hormones led to a refractory behavior of all parameters. Activation of the cAMP route could overcome this refractoriness. All agents caused CT, a measure of apical membrane area, to increase in a manner roughly synchronous with Gt. These results suggest that activation of the cAMP-messenger route may, at least partly, involve exocytosis of a vesicular Cl- channel pool. Apical flufenamate depressed Cl- current and conductance and apparently generated blocker-noise. However, blocking kinetics extracted from noise experiments could not be reconciled with those obtained from current inhibition, suggesting the drug does not act as simple open-channel inhibitor.

Animals↗