BackgroundEndotoxin (i.e. LPS) administration induces a robust inflammatory response with accompanying cardiovascular dysfunction and insulin resistance. Overabundance of nitric oxide (NO) contributes to the vascular dysfunction. However, inflammation itself also induces insulin resistance in skeletal muscle. We sought to investigate whether the cardiovascular dysfunction induced by increased NO availability without inflammatory stress can promote insulin resistance. Additionally, we examined the role of inducible nitric oxide synthase (iNOS or NOS2), the source of the increase in NO availability, in modulating LPS-induced decrease in insulin-stimulated muscle glucose uptake (MGU).MethodsThe impact of NO donor infusion on insulin-stimulated whole-body and muscle glucose uptake (hyperinsulinemic-euglycemic clamps), and the cardiovascular system was assessed in chronically catheterized, conscious mice wild-type (WT) mice. The impact of LPS on insulin action and the cardiovascular system were assessed in WT and global iNOS knockout (KO) mice. Tissue blood flow and cardiac function were assessed using microspheres and echocardiography, respectively. Insulin signaling activity, and gene expression of pro-inflammatory markers were also measured.ResultsNO donor infusion decreased mean arterial blood pressure, whole-body glucose requirements, and MGU in the absence of changes in skeletal muscle blood flow. LPS lowered mean arterial blood pressure and glucose requirements in WT mice, but not in iNOS KO mice. Lastly, despite an intact inflammatory response, iNOS KO mice were protected from LPS-mediated deficits in cardiac output. LPS impaired MGU in vivo, regardless of the presence of iNOS. However, ex vivo, insulin action in muscle obtained from LPS treated iNOS KO animals was protected.ConclusionNitric oxide excess and LPS impairs glycemic control by diminishing MGU. LPS impairs MGU by both the direct effect of inflammation on the myocyte, as well as by the indirect NO-driven cardiovascular dysfunction.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-015-0223-2) contains supplementary material, which is available to authorized users.
Background and Aims:Emergence time, or the duration between incision closure and extubation, is costly nonoperative time. Efforts to improve operating room efficiency and identify trainee progress make such time intervals of interest. We sought to calculate the incidence of prolonged emergence (i.e., >15 min) for patients under the care of clinical anesthesia (CA) residents. We also sought to identify factors from resident training, medical history, anesthetic use, and anesthesia staffing, which affect emergence.Material and Methods:In this single-center, historical cohort study, perioperative information management systems provided data for surgical cases under resident care at a tertiary care center in the United States from 2006 to 2008. Using multiple logistic regression, the effects of variables on emergence was analyzed.Results:Of 7687 cases under the care of 27 residents, the incidence of prolonged emergence was 13.9%. Emergence prolongation decreased by month in training for 1st-year (CA-1) residents (r2 = 0.7, P < 0.001), but not for CA-2 and CA-3 residents. Mean patient emergence time differed among 27 residents (P < 0.01 for 58.4% or 205/351 paired comparisons). In a model restricted to 1st-year residents, patient male gender, American Society of Anesthesiologists (ASA) physical status >II, emergency surgical case, operative duration ≥2 h, and paralytic agent use were associated with higher frequency of prolonged emergence, while sevoflurane or desflurane use was associated with lower frequency. Attending anesthesiologist handoff was not associated with longer emergence.Conclusion:Incidence of prolonged emergence from general anesthesia differed significantly among trainees, by resident training duration, and for patients with ASA >II.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.