Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2012
Salvinorin A pretreatment preserves cerebrovascular autoregulation after brain hypoxic/ischemic injury via extracellular signal-regulated kinase/mitogen-activated protein kinase in piglets.
Cerebral hypoxia/ischemia during infant congenital heart surgery is not uncommon and may induce devastating neurologic disabilities persistent over the lifespan. Hypoxia/ischemia-induced cerebrovascular dysfunction is thought to be an important contributor to neurological damage. No pharmacological agents have been found to prevent this. Mitogen activated protein kinase (MAPK), including extracellular signal regulated kinase (ERK), c-Jun-N-terminal kinase, and p38, is thought to contribute to ischemic preconditioning. We investigated whether pretreatment with salvinorin A, the only natural nonopioid κ receptor agonist, could preserve autoregulation of the pial artery via MAPK. ⋯ Salvinorin A pretreatment preserves autoregulation of the pial artery to hypotension and hypercapnia after hypoxia/ischemia via ERK in a piglet model.
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Anesthesia and analgesia · Jan 2012
Comparative StudyThe involvement of adenosine triphosphate-sensitive potassium channels in the different effects of sevoflurane and propofol on glucose metabolism in fed rats.
Recently, we reported marked differences in the effects of sevoflurane and propofol on glucose metabolism; glucose use is impaired by sevoflurane, but not by propofol. Opening of adenosine triphosphate-sensitive potassium channels (K(ATP) channels) in β islet cells attenuates insulin secretion, while inhibition of K(ATP) channels in β islet cells increases insulin secretion. It is reported that volatile anesthetics open K(ATP) channels, whereas propofol inhibits K(ATP) channels. In this study, we examined the effects of sevoflurane and propofol on glucose metabolism under normovolemic and hypovolemic conditions, focusing on insulin secretion. ⋯ Insulin secretion regulated by K(ATP) channels in β islet cells is involved, at least in part, in the different effects of sevoflurane and propofol on glucose metabolism.
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Anesthesia and analgesia · Jan 2012
Intravenous infusion of remifentanil induces transient withdrawal hyperalgesia depending on administration duration in rats.
Recent studies suggest that remifentanil, similar to other μ-opioid agonists, may induce hyperalgesia. We performed animal experiments to determine whether IV remifentanil infusion, the mode of administration used in clinical practice, induces hyperalgesia and the conditions in which this phenomenon occurs. We also determined whether remifentanil-induced hyperalgesia is related to extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation. ⋯ IV remifentanil induces transient withdrawal hyperalgesia soon after its termination. This hyperalgesia is strongly associated with the duration of exposure to remifentanil. Contrary to our hypothesis, ERK1/2 by itself was not the essential factor involved in the induction of the hyperalgesia.
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Anesthesia and analgesia · Jan 2012
Editorial Historical ArticleEducation in anesthesia: then & now.