Anesthesia and analgesia
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Anesthesia and analgesia · Jul 2017
Process Improvement Initiative for the Perioperative Management of Patients With a Cardiovascular Implantable Electronic Device.
Economic, personnel, and procedural challenges often complicate and interfere with efficient and safe perioperative care of patients with cardiovascular implantable electronic devices (CIEDs). In the context of a process improvement initiative, we created and implemented a comprehensive anesthesiologist-run perioperative CIED service to respond to all routine requests for perioperative CIED consultations at a large academic medical center. This study was designed to determine whether this new care model was associated with improved operating room efficiency, reduced institutional cost, and adequate patient safety. ⋯ Based on our experience, specially trained anesthesiologists can provide efficient and safe perioperative care for patients with CIEDs. Other centers may consider implementing a similar strategy as our specialty adopts the perioperative surgical home model.
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Anesthesia and analgesia · Jul 2017
Effects of Sevoflurane on Hemodynamics and Inducible Nitric Oxide Synthase/Soluble Guanylate Cyclase Signaling Pathway in a Rat Model of Pulmonary Arterial Hypertension.
The effects of sevoflurane on right ventricular (RV) function are incompletely understood. In a rat model of experimentally induced pulmonary arterial hypertension (PAH), we studied effects of sevoflurane on RV function and the expression of inducible nitric oxide synthase/soluble guanylate cyclase (iNOS/sGC) signaling pathway. We hypothesized that sevoflurane would improve RV function in rats with PAH via a iNOS/sGC pathway. ⋯ Sevoflurane depressed RV contractility to a lesser degree in PAH than in normal rats. Sevoflurane also upregulated iNOS expression and downregulated sGC expression in PAH, but not control rats. This observation may explain the differential effects of sevoflurane on RV function in rats with and without PAH.
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Anesthesia and analgesia · Jul 2017
Insufficient Astrocyte-Derived Brain-Derived Neurotrophic Factor Contributes to Propofol-Induced Neuron Death Through Akt/Glycogen Synthase Kinase 3β/Mitochondrial Fission Pathway.
Growing animal evidence demonstrates that prolonged exposure to propofol during brain development induces widespread neuronal cell death, but there is little information on the role of astrocytes. Astrocytes can release neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which can exert the protective effect on neurons in paracrine fashion. We hypothesize that during propofol anesthesia, BDNF released from developing astrocytes may not be sufficient to prevent propofol-induced neurotoxicity. ⋯ Astrocytes attenuate propofol-induced neurotoxicity through BDNF-mediated cell survival pathway suggesting multiple neuroprotective strategies such as administration of BDNF, astrocyte-conditioned medium, decreasing mitochondrial fission, or inhibition of GSK3β.