Anesthesiology
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Endotoxin causes acute lung injury, which can lead to acute respiratory distress syndrome. Because local anesthetics are known to attenuate inflammatory reactions, ropivacaine was tested for its possible antiinflammatory effect in lipopolysaccharide-induced lung injury in rat alveolar epithelial cells (AECs) and rat pulmonary artery endothelial cells (RPAECs) in vitro and in vivo. ⋯ Ropivacaine intervention substantially attenuated the inflammatory response in acute lung injury and thus may carry an interesting potential for antiinflammatory treatment.
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Myocardial protection by anesthetics is known to involve activation of protein kinase C (PKC). The authors' objective was to identify the PKC isoforms activated by propofol in rat ventricular myocytes. They also assessed the intracellular location of individual PKC isoforms before and after treatment with propofol. ⋯ These results demonstrate that propofol causes an increase in PKC activity in rat ventricular myocytes. Propofol stimulates translocation of PKC-alpha, PKC-delta, PKC-epsilon, and PKC-zeta to distinct intracellular sites in cardiomyocytes. This may be a fundamentally important cellular mechanism of anesthesia-induced myocardial protection in the setting of ischemia-reperfusion injury.
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Opioid-induced hyperalgesia (OIH) is a syndrome of increased sensitivity to noxious stimuli, seen after both the acute and chronic administration of opioids, that has been observed in humans and rodent models. This syndrome may reduce the clinical utility of opioids in treating acute and chronic pain. ⋯ Genetic variants of the beta2-AR gene seem to explain some part of the differences between various strains of mice to develop OIH. The association of this gene with OIH suggests specific pharmacologic strategies for reducing the impact of OIH on patients consuming opioids.