Anesthesiology
-
Comparative Study
Pro- versus Antinociceptive Nongenomic Effects of Neuronal Mineralocorticoid versus Glucocorticoid Receptors during Rat Hind Paw Inflammation.
In naive rats, corticosteroids activate neuronal membrane-bound glucocorticoid and mineralocorticoid receptors in spinal cord and periphery to modulate nociceptive behavior by nongenomic mechanisms. Here we investigated inflammation-induced changes in neuronal versus glial glucocorticoid and mineralocorticoid receptors and their ligand-mediated nongenomic impact on mechanical nociception in rats. ⋯ The enhanced mechanical sensitivity of inflamed hind paws accompanied with corticosteroid receptor upregulation in spinal and peripheral sensory neurons was attenuated immediately after glucocorticoid receptor agonist and mineralocorticoid receptor antagonist administration, suggesting acute nongenomic effects consistent with detected membrane-bound corticosteroid receptors.
-
Observational Study
Simulation-based Assessment to Reliably Identify Key Resident Performance Attributes.
Obtaining reliable and valid information on resident performance is critical to patient safety and training program improvement. The goals were to characterize important anesthesia resident performance gaps that are not typically evaluated, and to further validate scores from a multiscenario simulation-based assessment. ⋯ Sensitivity of the assessment to CA-1 versus CA-3 performance differences for most scenarios and domains supports validity. No differences, by experience level, were detected for two domains associated with reflective practice. Smaller score variances for CA-3s likely reflect a training effect; however, worrisome performance scores for both CA-1s and CA-3s suggest room for improvement.
-
Anesthetics in ventilated patients are critical as any cofactor hampering diaphragmatic function may have a negative impact on the weaning progress and therefore on patients' mortality. Dexmedetomidine may display antioxidant and antiproteolytic properties, but it also reduced glucose uptake by the muscle, which may impair diaphragm force production. This study tested the hypothesis that dexmedetomidine could inhibit ventilator-induced diaphragmatic dysfunction. ⋯ Twenty-four hours of mechanical ventilation during dexmedetomidine sedation led to a worsening of ventilation-induced diaphragm dysfunction, possibly through impaired Glut-4 translocation. Although dexmedetomidine prevented diaphragmatic fiber atrophy, it did not inhibit oxidative stress and activation of the proteolytic pathways.