Anesthesiology
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Ischemia causes an imbalance in mitochondrial metabolism and accumulation of nicotinamide adenine dinucleotide (NADH). We showed that anesthetic preconditioning (APC), like ischemic preconditioning, improved mitochondrial NADH energy balance during ischemia and improved function and reduced infarct size on reperfusion. Opening adenosine triphosphate-sensitive potassium (K(atp)) channels may be involved in triggering APC. The authors tested if effects of APC on NADH concentrations before, during, and after ischemia are reversible by 5-hydroxydecanoate (5-HD), a putative mitochondrial K channel blocker. ⋯ Anesthetic preconditioning was evidenced by improved mitochondrial bioenergetics as assessed from NADH concentrations during ischemia and by attenuated reperfusion injury. Reversal of APC by bracketing sevoflurane exposure with 5-HD suggests that APC is triggered by mitochondrial K channel opening or, alternatively, by attenuated mitochondrial respiration without direct involvement of mitochondrial K channel opening.
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Neuromuscular blockade at the laryngeal adductor muscles may be measured using the cuff of a endotracheal tube placed between the vocal cords. Phonomyography is an alternative method of neuromuscular monitoring. In this study, phonomyography is applied to determine blockade at the larynx and compared with the cuff pressure method. ⋯ Both methods can be used interchangeably to determine neuromuscular blockade of the laryngeal adductor muscles. Phonomyography allows measurement of laryngeal blockade with the endotracheal tube in the normal position.
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The authors investigated whether the sedative, or hypnotic, action of the general anesthetic dexmedetomidine (a selective alpha -adrenoceptor agonist) activates endogenous nonrapid eye movement (NREM) sleep-promoting pathways. ⋯ The authors propose that endogenous sleep pathways are causally involved in dexmedetomidine-induced sedation; dexmedetomidine's sedative mechanism involves inhibition of the LC, which disinhibits VLPO firing. The increased release of GABA at the terminals of the VLPO inhibits TMN firing, which is required for the sedative response.
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Randomized Controlled Trial Multicenter Study Comparative Study Clinical Trial
Prospective study on incidence and functional impact of transient neurologic symptoms associated with 1% versus 5% hyperbaric lidocaine in short urologic procedures.
The objectives of this study were to compare the incidence, onset, duration and pain scores of transient neurologic symptoms (TNS) with 1% versus 5% hyperbaric lidocaine in spinal anesthesia for short urological procedures in a large prospective study. This study would also evaluate patient satisfaction, and impact of TNS on functional recovery to assess the clinical significance of TNS. ⋯ There was no difference in the incidence of TNS between the 1% versus 5% spinal lidocaine groups. Pain scores were higher in patients with TNS than those who did not have TNS. During the first 48 h postop, a small proportion of patients who had TNS experienced functional impairment of walking, sitting, and sleeping.