[Supplemental oxygen for the prevention of postoperative nausea and vomiting: a meta-analysis of randomized clinical trials]. / Oxígeno suplementario para la prevención de la náusea y el vómito postoperatorios: Meta-análisis de experimentos clínicos aleatorizados.

OBJECTIVE: Despite the development of antiemetic drugs, the incidence of postoperative nausea and vomiting remains between 20% and 30%. This meta-analysis examines the hypothesis that perioperative administration of supplemental oxygen reduces the incidence of these complications. METHODS: We performed a systematic search of the literature through MEDLINE, EMBASE, the Cochrane Library, reference lists, and a manual search, with no language restrictions, up to September 2007 to identify randomized clinical trials evaluating the effect o f supplemental oxygen on postoperative nausea and vomiting. The data were extracted and analyzed using the RevMan program, version 4.2.9 (Cochrane Collaboration, Oxford, UK). RESULTS: The study included 9 randomized clinical trials with a total of 1661 enrolled patients (824 assigned to the group with a higher oxygen concentration and 837 assigned to the group with a lower oxygen concentration). Perioperative supplemental oxygen has no effect on the incidence of nausea (relative risk [RR], 0.94; 95% confidence interval [CI], 0.82 to 1.08), postoperative nausea and/or vomiting (RR, 0.93; 95% CI, 0.74 to 1.17), or the need for rescue antiemetic drugs (RR, 0.90; 95% CI, 0.70 to 1.15). The incidence of vomiting, however, is reduced (RR, 0.77; 95% CI, 0.62 to 0.97). Significant differences were not found in the incidence of atelectasis (RR, 1.23; 95% CI, 0.50 to 3.00) or postoperative PaCO2 (weighted mean difference, -4.0; 95% CI, -12.3 to 4.3). CONCLUSIONS: Supplemental oxygen reduces the incidence of postoperative vomiting. Administration of supplemental oxygen could be an effective method of reducing postoperative vomiting but does not replace current indications for pharmacologic prophylaxis.

[Construction and validation of a model to predict intraoperative hypothermia]. / Construcción y validación de un modelo predictivo de hipotermia intraoperatoria.

OBJECTIVES: Perioperative hypothermia is linked to adverse effects that increase morbidity and mortality. The objectives of this study were to identify the risk factors for intraoperative hypothermia and construct an instrument for identifying patients at high risk. MATERIALS AND METHODS: We studied patients of all ages who had undergone surgery. Patients were assigned to a design group or a validation group by means of a list of randomly generated numbers. Intraoperative hypothermia was defined by an tympanic temperature of 35.9 degrees C or less. A bivariate analysis of the design group identified the predictive factors and a multivariate analysis (logistic regression with backward elimination of nonsignificant variables) provided a predictive model. Risk scores were obtained for each variable by converting them to a 4-degree risk scale (abbreviated model). Predictive power was determined by calculating the area under the receiver-operator characteristic curve (AUC). RESULTS: We enrolled 264 consecutive patients; 200 were assigned to the design group and 64 to the validation group. In the design group, the AUC was 0.85 for the complete model and 0.83 for the abbreviated model. In the validation group, the AUC was 0.85 for the complete model and 0.82 for the abbreviated model. The P value was <.01 for all curves. CONCLUSION: Age, weight, approximate duration of surgery, and body and ambient temperature during induction were the included factors that predicted intraoperative hypothermia in a heterogeneous sample of surgical patients.

The binding of near-ultraviolet light-induced tryptophan photoproduct(s) to DNA.

To test one possible mode of toxicity of L-tryptophan photoproduct(s) to bacterial cells, we have examined the binding of near-ultraviolet light-treated tryptophan to purified Escherichia coli DNA in vitro. The results show that co-irradiated (or pre-irradiated) [3H]tryptophan binds to purified DNA as assayed by trichloroacetic acid co-precipitation of DNA and 3H counts on cellulose filters. This was supported by co-sedimentation of DNA and 3H photoproduct(s) on CsCl gradients. Hot trichloroacetic acid extraction or enzymatic digestion of DNA prevents filter binding. The binding is most efficient when tryptophan and DNA are co-irradiated. Under these conditions, binding is more efficient with denatured rather than native DNA. From kinetic studies, the binding is DNA-dependent at constant doses of near-ultraviolet light. At a dose of 2.16 - 10(6) ergs - mm-2 we estimate that 100-150 L-[3H]tryptophan equivalents are bound per E. coli genome equivalent. The binding does not occur with another aromatic amino acid such as tyrosine.

Features of the damage produced by proflavine on transforming deoxyribonucleic acid.

Proflavine formed a complex with transforming deoxyribonucleic acid (DNA) from Haemophilus influenzae, with optimal formation at a ratio of proflavine to DNA of 0.06. The rate of dissociation of the complex by dialysis increased in the order: native, denatured, renatured DNA. The transforming activity of the DNA was reduced by its interaction with proflavine. This inactivation was dependent on the physical state of the DNA, the proflavine concentration, and the temperature. DNA that had been denatured and renatured was most sensitive; native DNA was much less sensitive. The inactivation remained after dialysis and was stable to prolonged storage. It is concluded that the inactivation of transforming DNA by proflavine takes place by a mechanism different from that of DNA-proflavine complex formation.

Lethal and mutagenic action of hydrogen peroxide on Haemophilus influenzae.

The lethal and mutagenic effects of H2O2 on wild-type Haemophilus influenzae Rd and on uvr1, uvr2, rec1, and rec2 mutant strains were studied. The first two mutants are sensitive to UV, and the second two are defective in recombination. Rd, urv1, and rec1 strains were more sensitive to the killing effect of H2O2 treatment than were uvr2 and rec2 strains. There were peaks of mutagenesis at two H2O2 concentrations over a range of 30 to 275 mM. Our results suggest a specific repair of H2O2 damage that is independent of the Uvr2 and Rec2 gene products. Sensitivity to the killing effect of H2O2 and to the lethal action of near-UV light were similar for Rd and uvr1 strains. This finding suggests that the mechanisms of killing by and repair of H2O2 damage may have some overlap with those of near-UV radiation.