Journal of anesthesia
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Journal of anesthesia · Oct 2014
ReviewCellular signaling pathways and molecular mechanisms involving inhalational anesthetics-induced organoprotection.
Inhalational anesthetics-induced organoprotection has received much research interest and has been consistently demonstrated in different models of organ damage, in particular, ischemia-reperfusion injury, which features prominently in the perioperative period and in cardiovascular events. The cellular mechanisms accountable for effective organoprotection over heart, brain, kidneys, and other vital organs have been elucidated in turn in the past two decades, including receptor stimulations, second-messenger signal relay and amplification, end-effector activation, and transcriptional modification. ⋯ The salubrious effects of inhalational anesthetics on vital organs, if reproducible in human subjects in clinical settings, would be of exceptional clinical importance, but clinical studies with better design and execution are prerequisites for valid conclusions to be made. Xenon as the emerging inhalational anesthetic, and its organoprotective efficacy, mechanism, and relative advantages over other anesthetics, are also discussed.
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The nociceptin system comprises the nociceptin receptor (NOP) and the ligand nociceptin/orphanin FQ (N/OFQ) that binds to the receptor. The archetypal role of the system is in pain processing but the NOP receptor is also expressed on immune cells. ⋯ As there is a loss of regulation of inflammatory responses during sepsis, the nociceptin system could be a target for therapies aimed at modulating sepsis. This review details the known effects of NOP activation on leucocytes and the vascular endothelium and discusses the most recent human and animal data on the role of the nociceptin system in sepsis.
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Journal of anesthesia · Oct 2014
Clinical evaluation of hyponatremia and hypovolemia in critically ill adult neurologic patients: contribution of the use of cumulative balance of sodium.
Knowledge of the cumulative balance of sodium (CBS) is important for the diagnosis of salt disorders and water homeostasis and has the potential to predict hypovolemic status in acute neurological patients. However, an extensive application of the use of CBS is still lacking in the intensive care setting, where salt and water homeostasis represents a priority. ⋯ CBS is likely to be a useful parameter in the diagnosis of CSWS and a surrogate parameter for estimating hypovolemia in acute neurological patients.
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Journal of anesthesia · Oct 2014
Preventive effects of multisensory rehabilitation on development of cognitive dysfunction following systemic inflammation in aged rats.
Systemic inflammation can trigger transient or longer-lasting cognitive impairments, particularly in elderly patients. However, its pathogenesis has not been sufficiently clarified. In this study, we explored the potential effects of multisensory rehabilitation on cognitive dysfunction following systemic inflammation using an animal model. ⋯ These memory deficits were positively correlated with the levels of both tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the hippocampus. On the other hand, in the LPS-treated ER group, neither cognitive impairment nor an increase in hippocampal levels of both TNF-α and IL-1β was found. These results imply that early rehabilitation (ER) intervention may be effective in preventing cognitive dysfunction following systemic inflammation via its anti-neuroinflammatory effects.
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Journal of anesthesia · Oct 2014
Potentiation of [Met(5)]enkephalin-induced antinociception by mixture of three peptidase inhibitors in rat.
Previous in vitro studies have shown that degradation of opioid peptides during incubation with cerebral membrane preparations is almost completely prevented by a mixture of three peptidase inhibitors (PIs), namely, amastatin, captopril, and phosphoramidon. In the present in vivo study, we evaluate the effects of intrathecal administration of these PIs on antinociception by [Met(5)]enkephalin (ME) or PIs themselves. ⋯ The present data, together with those of earlier studies, clearly demonstrate that amastatin-, captopril-, and phosphoramidon-sensitive enzymes play an important role in inactivation of opioid peptides at the spinal level.