BackgroundRoutine hemodynamic monitoring parameters under general anesthesia, such as heart rate (HR), systolic blood pressure (SBP), and perfusion index (PI), do not solely reflect intraoperative nociceptive levels. We developed a hemodynamic model combining these 3 parameters for nociceptive responses during general anesthesia, and evaluated nociceptive responses to surgical skin incision.Material/MethodsWe first retrospectively performed discriminant analysis using 3 values – HR, SBP, and PI – to assess response to skin incision during tympanoplasty, laparoscopic cholecystectomy, and open gastrectomy to determine if combined use of these parameters differentiates nociceptive levels among these 3 surgeries. Secondly, ordinal logistic regression analysis was applied using the 3 parameters to develop an equation representing nociceptive response during general anesthesia, and then evaluated its utility to discern nociceptive responses to skin incision.ResultsWe developed the following hemodynamic model as calculated nociceptive response= −1+2/(1+ exp(−0.01 HR −0.02 SBP +0.17 PI)), and prospectively determined that calculated nociceptive responses to small skin incision for laparoscopic surgery were significantly lower than responses to large skin incision for laparotomy.ConclusionsOur hemodynamic model using HR, SBP, and PI likely reflects nociceptive levels at skin incision during general anesthesia, and quantitatively discerned the difference in nociceptive responses to skin incision between laparoscopy and laparotomy. This model could be applicable to assess either real-time nociceptive responses or averaged nociceptive responses throughout surgery without using special equipment.

We conclude that the AWS is an effective device for endotracheal intubation during chest compression not only on the bed but also on the ground.

Oxidative stress induces mitochondrial dysfunction and facilitates apoptosis, tissue damage or metabolic alterations following infection. We have previously discovered that the Pseudomonas aeruginosa (PA) quorum sensing (QS)-excreted small volatile molecule, 2-aminoacetophenone (2-AA), which is produced in infected human tissue, promotes bacterial phenotypes that favor chronic infection, while also compromising muscle function and dampens the pathogen-induced innate immune response, promoting host tolerance to infection. In this study, murine whole-genome expression data have demonstrated that 2-AA affects the expression of genes involved in reactive oxygen species (ROS) homeostasis, thus producing an oxidative stress signature in skeletal muscle. The results of the present study demonstrated that the expression levels of genes involved in apoptosis signaling pathways were upregulated in the skeletal muscle of 2-AA-treated mice. To confirm the results of our transcriptome analysis, we used a novel high-resolution magic-angle-spinning (HRMAS), proton (1H) nuclear magnetic resonance (NMR) method and observed increased levels of bisallylic methylene fatty acyl protons and vinyl protons, suggesting that 2-AA induces skeletal muscle cell apoptosis. This effect was corroborated by our results demonstrating the downregulation of mitochondrial membrane potential in vivo in response to 2-AA. The findings of the present study indicate that the bacterial infochemical, 2-AA, disrupts mitochondrial functions by inducing oxidative stress and apoptosis signaling and likely promotes skeletal muscle dysfunction, which may favor chronic/persistent infection.

To compare tracheal intubation with the Pentax Airway Scope (AWS) and the Macintosh laryngoscope (McL) during chest compression, 25 anesthesiologists (including 12 specialists having >5 years of experience and 13 trainees having <2 years of experience) performed tracheal intubation using either the McL or the AWS, with or without chest compression, on a manikin. Using the McL, both specialists and trainees took a significantly longer time (P < 0.01) to secure the airway with chest compression (17.3 +/- 3.7 and 22.5 +/- 8.0, respectively) and than without chest compression (11.3 +/- 2.9 and 13.9 +/- 4.4 s, respectively). No significant difference was observed in time needed to secure the airway using the AWS with or without chest compression in both groups. From the standpoint of experience, time to complete intubation for specialists using the McL during chest compression was significantly shorter than that for trainees. In contrast, the difference in time to complete intubation with the AWS during chest compression was not significantly different between the two groups. Based on these results, we conclude that the use of the AWS may reduce the time needed to secure the airway during chest compression.