Anesthesiology
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Comment Letter
Learning disabilities may be related to undetected hypoxia.
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The authors compared the neuroprotective effects induced by two ischemic postconditioning methods and sought to determine the roles of phosphatidylinositol 3-kinase-Akt and extracellular signal-regulated kinase (ERK) in this neuroprotection. ⋯ The two postconditioning methods possess comparable neuroprotective effects on the spinal cord and share a common molecular mechanism, in which phosphatidylinositol 3-kinase and ERK pathways play crucial roles.
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Acute hypercapnic acidosis protects against lung injury caused by nonseptic insults and after both pulmonary and systemic sepsis. The authors wished to dissect the contribution of the acidosis versus hypercapnia per se to the effects of hypercapnic acidosis on the hemodynamic profile and severity of lung injury induced by systemic sepsis. ⋯ Both hypercapnic acidosis and buffered hypercapnia attenuate the hemodynamic consequences of systemic sepsis. In contrast, hypercapnic acidosis, but not buffered hypercapnia, reduced the severity of sepsis-induced lung injury.
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Ischemic preconditioning (IPC) and anesthetic-induced preconditioning against myocardial infarction are mediated via protein kinase B. Pim-1 kinase acts downstream of protein kinase B and was recently shown to regulate cardiomyocyte survival. The authors tested the hypothesis that IPC and anesthetic-induced preconditioning are mediated by Pim-1 kinase. ⋯ These data suggest that Pim-1 kinase mediates at least in part desflurane-induced preconditioning and IPC against myocardial infarction in mice.