Anesthesiology
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In myasthenic patients, the sensitivity for nondepolarizing relaxants is increased and the time course of effect is prolonged due to a reduced number of functional acetylcholine receptors at the neuromuscular junction. The authors investigated both the performance of the link model proposed by Sheiner and a pharmacodynamic-pharmacokinetic model taking into account the number of unbound acetylcholine receptors in myasthenic pigs. ⋯ Both the Sheiner model and the unbound receptor model may be used to fit plasma concentration-effect data of rocuronium in pigs. The unbound receptor concentration model, however, can explain the observed differences in the time course of effect, based on receptor concentration.
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Comparative Study
Comparison of the visceral antinociceptive effects of spinally administered MPV-2426 (fadolmidine) and clonidine in the rat.
The authors determined the visceral antinociceptive effect induced by MPV-2426 (fadolmidine), a selective alpha 2 -adrenoceptor agonist, in rats with and without inflammation of the colon. They also determined whether the sympathetic nervous system or intact descending pathways are critical for the alpha 2 -adrenoceptor-induced visceral antinociception. ⋯ Spinally administered MPV-2426 produces a dose-dependent visceral antinociception as well in animals with an inflammation of the colon as in controls. The visceral antinociceptive effect induced by spinal MPV-2426 is equipotent to that of spinal clonidine. An intact sympathetic nervous system or intact brainstem-spinal pathway is not critical for the MPV-2426-induced visceral antinociception.
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Knowledge of the influence of age on laryngeal dimensions is essential for all practitioners whose interest is the pediatric airway. Early cadaver studies documented that the larynx is conically shaped, with the apex of the cone caudally positioned at the nondistensible cricoid cartilage. These dimensions change during childhood, as the larynx assumes a more cylindrical shape. The authors analyzed laryngeal dimensions during development to determine if this relationship continues in unparalyzed children in whom laryngeal muscles are tonically active. The authors determined the relationships between the vocal cord, sub-vocal cord, and cricoid ring dimensions and the influence of age on these relationships. ⋯ In sedated, unparalyzed children, the narrowest portions of the larynx are the glottic opening (vocal cord level) and the immediate sub-vocal cord level, and there is no change in the relationships of these dimensions relative to cricoid dimensions throughout childhood.
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Systemic lidocaine and other local anesthetics reduce hypersensitivity states induced by both acute inflammation and peripheral nerve injury in animals and produce analgesia in some patients with chronic pain. The mechanisms underlying the antiallodynic effect of systemic lidocaine are unclear, although most focus is on peripheral mechanisms. Central mechanisms, particularly at the spinal dorsal horn level, are less known. In this study, the authors aimed to determine whether intrathecal lidocaine has an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models: partial sciatic nerve ligation (PSNL) and spinal nerve ligation (SNL). ⋯ The authors' data suggest that intrathecal lidocaine possibly suppressed the hyperexcitability of the dorsal horn neurons and likely interacted with eicosanoid systems in the spinal dorsal horn.
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Adding epinephrine to lidocaine solutions for peripheral nerve block potentiates and prolongs the action, but by incompletely understood mechanisms. In an effort to discriminate the pharmacokinetic from the pharmacodynamic effects of epinephrine, the authors measured the lidocaine content of peripheral nerve over the course of block produced by 0.5% lidocaine, with and without epinephrine, and correlated it with the degree of analgesia. ⋯ Adding epinephrine to lidocaine solutions increases the intensity and duration of sciatic nerve block in the rat. The early increase in intensity is not matched with an increase in intraneural lidocaine content at these early times, although the prolonged duration of block by epinephrine appears to correspond to an enlarged lidocaine content in nerve at later times, as if a very slowly emptying "effector compartment" received a larger share of the dose. The increase in early analgesia without increased lidocaine content may be explained by a pharmacodynamic action of epinephrine that transiently enhances lidocaine's potency, but also by a pharmacokinetic effect that alters the distribution of the same net content of lidocaine within the nerve.