PubMed · 10366277
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R Walker, O R Dearlove, I Aguilera. 1999. Post tonsillectomy pain.. https://doi.org/10.1046/j.1460-9584.1999.00387.x
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The electroanalytical study of ascorbic acid, acetaminophen and of several mixtures of these compounds in different ratios has been made by using a carbon paste electrode (CPE-graphite:solid paraffin 2:1) as working electrode and an Ag/AgCl reference electrode. The potential curves were recorded using different concentrations of ascorbic acid and acetaminophen by measuring samples between 10 and 50 microl. The oxidation reactions were studied in a potential range from -0.1 to +1.3 V with different sweep rates, at different current sensitivities, in stationary working conditions and stirring before each replicate. The oxidation of ascorbic acid occurs at +0.31 +/- 0.02 V and the oxidation of acetaminophen at +0.60 +/- 0.05 V; meanwhile, the current has a linear variation for the following concentration ranges: 10(-3)-10(-2) M for the ascorbic acid and 3 x 10(-6)-7.5 x 10(-3) M for acetaminophen (r2 = 0.999 for both ascorbic acid and acetaminophen). The mixtures of ascorbic acid and acetaminophen were made as follows: 1:1, 1:2, 1:3, 2:1, and 3:1. The studies revealed the alteration of the voltammograms processed according to the validation methodology. The best potential variation range for different current sensitivities, the influence of the sweep rate, of the solvent volume and of the pH were studied. The mutual interferences of the compounds in the mixtures and the electroactive compounds in the pharmaceutical dosage forms, especially effervescent ones, also made the object of the research. The same mixtures were studied using the direct spectrophotometric method that revealed a lot of spectral interferences. In order to solve this problem, an appropriate separation or an indirect spectrophotometric method (the apparent content curves method) were used. The spectrophotometric and voltammetric methods developed were used to determine ascorbic acid and acetaminophen in different dosage forms (vials, tablets, suppositories and effervescent dosage forms). The results were compared with those obtained by other techniques.
Post-operative pain is frequently measured by a visual analogue scale (VAS). The most common methods for analysing such data are the so-called time-by-time method and repeated measures analysis of variance. In the first, due to correlation between time points, successive tests are not independent and cannot measure the treatment effects over time. In the second, a rather unlikely covariance structure has to be assumed. In a simulation study we have shown that the power of the antedependence test is nearly the same as that of repeated measures of analysis of variance and it does not suffer from some of the latter's shortcomings. We also present an analysis of real data using the antedependence test.
Bacterial endotoxin (lipopolysaccharide, LPS) is known to potentiate the toxicity of many hepatotoxicants. However, exposure to a sublethal dose of LPS renders animals tolerant to a lethal dose of LPS, and protects against the toxicity of some chemicals. This study was designed to examine the effects of LPS pretreatment on acetaminophen- and carbon tetrachloride (CCl(4))-induced liver injury in LPS-sensitive C3H/OuJ and LPS-resistant C3H/HeJ mice. Pretreatment of male C3H/OuJ mice with a single injection of LPS (0. 1 mg/kg, ip, for 24 h) protected against the hepatotoxic effects of acetaminophen (400 mg/kg) and carbon tetrachloride (CCl(4), 30 mg/kg), as indicated by serum alanine aminotransferase activity. In contrast, pretreatment of C3H/HeJ mice with 0.1 or 10 mg/kg LPS afforded no protection against the hepatotoxic effects of acetaminophen and CCl(4). In an attempt to determine the mechanism of LPS-induced protection against acetaminophen- and CCl(4)-induced hepatotoxicity in C3H/OuJ mice, liver cytochrome P450 was determined 24 h after LPS injection. LPS treatment caused a 26% decrease in total P450 content in C3H/OuJ but not in C3H/HeJ mice. CYP3A-catalized testosterone 6 beta-, 2 beta-, and 15 beta-hydroxylation was decreased 40% by LPS only in C3H/OuJ mice. To determine whether the differences to LPS-response in the two stains of mice is mediated by a strain-related difference in the release of cytokines, mice were pretreated with interleukin-1 (IL-1 alpha, 5 x 10(5) U/mouse), and the hepatoprotection and hepatic P450 enzymes were examined. IL-1 alpha pretreatment equally protected against the hepatotoxicity of acetaminophen and CCl(4) in both strains, and suppressed the total microsomal P450 and P450 enzyme-catalyzed testosterone hydroxylation to a similar extent. In conclusion, LPS pretreatment suppressed hepatic cytochrome P450 enzymes and protected against the hepatotoxicity of acetaminophen and CCl(4) in LPS-sensitive C3H/OuJ mice, but not in LPS-refractory C3H/HeJ mice. This protective effect of LPS appears to be mediated through the release of cytokines such as IL-1 alpha, which in turn suppresses the cytochrome P450 responsible for the activation of acetaminophen and CCl(4) to reactive metabolites.