Anesthesiology
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Volatile anesthetics precondition against myocardial infarction, but it is unknown whether this beneficial action is threshold- or dose-dependent. The authors tested the hypothesis that isoflurane decreases myocardial infarct size in a dose-dependent fashion in vivo. ⋯ Concentrations of isoflurane as low as 0.25 MAC are sufficient to precondition myocardium against infarction. High concentrations of isoflurane may have greater efficacy to protect myocardium during conditions of low coronary collateral blood flow.
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Clinical Trial
Inability to consistently elicit a motor response following sensory paresthesia during interscalene block administration.
Two methods of nerve block based on eliciting neural feedback with the block needle currently exist. The paresthesia technique uses sensory feedback to ascertain that the needle tip is close to the nerve. By contrast, a peripheral nerve stimulator makes use of motor responses to electrical stimulation. The relation of motor responses to an electrical peripheral nerve stimulator and sensory nerve contact (paresthesia) had not been studied. ⋯ Elicitation of paresthesia does not translate to an ability to elicit a motor response to a peripheral nerve stimulator in the majority of patients.
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General anesthetics can modulate the 5-hydroxytryptamine type 3 (5-HT3) receptor, which may be involved in processes mediating nausea and vomiting, and peripheral nociception. The effects of the new volatile anesthetic sevoflurane and the gaseous anesthetics nitrous oxide (N2O) and xenon (Xe) on the 5-HT3 receptor have not been well-characterized. ⋯ Inhalational general anesthetics produce diverse effects on the 5-HT3 receptor. Both halothane and isoflurane enhanced 5-HT3 receptor function in a concentration-dependent manner, which is consistent with previous studies. Sevoflurane inhibited the 5-HT3 receptor noncompetitively, whereas N2O and Xe inhibited the 5-HT3 receptor competitively, suggesting the inhibitory mechanism of sevoflurane might be different from those of N2O and Xe.
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After a focal thermal injury to the heel of a rat, thermal hyperalgesia appears at the injury site (primary thermal hyperalgesia), and tactile allodynia appears at the off-injury site (secondary tactile allodynia). The pharmacology of spinal glutamatergic receptors in the initiation and maintenance of secondary tactile allodynia was examined. ⋯ Spinal AMPA-KA receptors play a major role in the initiation of secondary tactile allodynia induced by focal thermal injury. In contrast, spinal NMDA receptors play only a minimal role.