Anesthesiology
-
Comparative Study
Isoflurane enhances both fast and slow synaptic inhibition in the hippocampus at amnestic concentrations.
Inhibition mediated by γ-aminobutyric acid type A (GABA A) receptors has long been considered an important target for a variety of general anesthetics. In the hippocampus, two types of phasic GABA A receptor-mediated inhibition coexist: GABA A,fast, which is expressed primarily at peri-somatic sites, and GABAA,slow, which is expressed primarily in the dendrites. Their spatial segregation suggests distinct functions: GABA A,slow may control plasticity of dendritic synapses, whereas GABA A,fast controls action potential initiation at the soma. We examined modulation of GABA A,fast and GABA A,slow inhibition by isoflurane at amnesic concentrations, and compared it with modulation by behaviorally equivalent doses of the GABA A receptor-selective drug etomidate. ⋯ Isoflurane enhances both types of phasic GABA A receptor-mediated inhibition to similar degrees at amnesic concentrations. This pattern differs from etomidate, which at low concentrations selectively enhances slow inhibition. These effects of isoflurane are sufficiently large that they may contribute substantially to its suppression of hippocampal learning and memory.
-
Comparative Study
Systematic criteria for type and screen based on procedure's probability of erythrocyte transfusion.
At many hospitals, the type and screen decision is guided by the hospital's maximum surgical blood order schedule, a document that includes for each scheduled (elective) surgical procedure a recommendation of whether a preoperative type and screen be performed. There is substantial heterogeneity in the scientific literature for how that decision should be made. ⋯ We validated a method to determine procedures on the maximum surgical blood order schedule for which type and screen was not indicated using the estimated blood losses and incidences of transfusion.
-
Comparative Study
Anesthetic propofol causes glycogen synthase kinase-3β-regulated lysosomal/mitochondrial apoptosis in macrophages.
Overdose propofol treatment with a prolong time causes injury to multiple cell types; however, its molecular mechanisms remain unclear. Activation of glycogen synthase kinase (GSK)-3β is proapoptotic under death stimuli. The authors therefore hypothesize that propofol overdose induces macrophage apoptosis through GSK-3β. ⋯ These results suggest an essential role of GSK-3β in propofol-induced lysosomal/mitochondrial apoptosis.