Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2011
Ketamine activates the L-arginine/Nitric oxide/cyclic guanosine monophosphate pathway to induce peripheral antinociception in rats.
The involvement of the L-arginine/nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway in antinociception has been implicated as a molecular mechanism of antinociception produced by several antinociceptive agents, including μ-, κ-, or δ-opioid receptor agonists, nonsteroidal analgesics, cholinergic agonist, and α2C adrenoceptor agonist. In this study, we investigated whether ketamine, a dissociative anesthetic N-methyl-D-aspartate receptor antagonist, was also capable of activating the L-arginine/NO/cGMP pathway and eliciting peripheral antinociception. ⋯ Our results suggest that ketamine stimulates the L-arginine/NO/cyclic GMP pathway via neuronal NO synthase to induce peripheral antinociceptive effects.
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Anesthesia and analgesia · Nov 2011
Limb remote postconditioning alleviates cerebral reperfusion injury through reactive oxygen species-mediated inhibition of delta protein kinase C in rats.
Remote ischemic postconditioning (RPostC) is an emerging concept for cerebral infarction protection, and its potential protective mechanisms have not been well established. We attempted to investigate the implications of reactive oxygen species (ROS) and δ protein kinase C (δPKC) in neuroprotection induced by RPostC in a rat model of focal cerebral ischemia, and also to explore a possible relationship between ROS and εPKC. ⋯ These findings suggested that RPostC performed in one limb alleviated reperfusion injury after focal cerebral ischemia through ROS-mediated inhibition of endogenous δPKC activation signaling cascade in an in vivo rat model of focal cerebral ischemia.
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Anesthesia and analgesia · Nov 2011
GABAergic excitotoxicity injury of the immature hippocampal pyramidal neurons' exposure to isoflurane.
Certain anesthetics exhibit neurotoxicity in the brains of immature but not mature animals. γ-Aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the adult brain, is excitatory on immature neurons via its action at the GABAA receptor, depolarizing the membrane potential and inducing a cytosolic Ca2+ increase ([Ca2+]i), because of a reversed transmembrane chloride gradient. Recent experimental data from several rodent studies have demonstrated that exposure to isoflurane during an initial phase causes neuronal excitotoxicity and apoptosis. GABAA receptor-mediated synaptic voltage-dependent calcium channels' (VDCCs) overactivation and Ca2+ influx are involved in these neural changes. ⋯ Isoflurane-mediated enhancement of GABA-triggered [Ca2+]i release results from membrane depolarization with subsequent activation of VDCCs and further Ca2+-induced Ca2+ release from the ryanodine-sensitizing Ca2+ store. An increase in [Ca2+]i, caused by activation of the GABAA receptor and opening of VDCCs, is necessary for isoflurane-induced calcium overload of immature rat hippocampal neurons, which may be involved in the mechanism of an isoflurane-induced neurotoxic effect in the developing rodent brain.