Anesthesiology
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Randomized Controlled Trial Clinical Trial
Enzymatic antagonism of mivacurium-induced neuromuscular blockade by human plasma cholinesterase.
Mivacurium chloride is a bis-benzylisoquinolinium nondepolarizing neuromuscular blocking agent, hydrolyzed by butyrylcholinesterase (PCHE). The dose-response relationships for PCHE after mivacurium have not been studied. Therefore, this study was designed to establish dose-response relationships for PCHE as an antagonist of mivacurium-induced neuromuscular blockade. ⋯ Administration of exogenous PCHE equivalent to activity present in 25 ml/kg of human plasma (in a 65-kg patient, this dose is equivalent to PCHE activity of 1,625 ml of adult human plasma) resulted in reliable antagonism of mivacurium-induced neuromuscular blockade. Nevertheless, because of the prohibitive cost of this compound, this reversal modality is unlikely to have a routine practical application at this time.
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The application of phase-modulated near-infrared techniques for measurement of the oxygen saturation of cerebral tissue requires both validation by conventional measures of cerebral oxygenation and determination of normal and abnormal values. This study was undertaken to validate phase-modulated near-infrared measurements of cerebral oxygen saturation by comparing them with electroencephalographic evidence of cerebral ischemia during implantation of cardioverting defibrillators. This comparison also yields an estimate of the ischemic threshold as measured with near-infrared techniques. ⋯ Near-infrared measurements reflect changes in cerebral oxygenation as indicated by electroencephalographic evidence of cerebral ischemia.
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Review Case Reports
Severe neurologic deficit after nitrous oxide anesthesia.
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Randomized Controlled Trial Clinical Trial
Influence of high-dose aprotinin on anticoagulation, heparin requirement, and celite- and kaolin-activated clotting time in heparin-pretreated patients undergoing open-heart surgery. A double-blind, placebo-controlled study.
Aprotinin causes a prolongation of the celite-activated clotting time (CACT), but not of the kaolin-activated clotting time (KACT). Therefore, concern has been raised regarding the reliability of CACT to monitor anticoagulation in the presence of aprotinin. The current study was designed to test the efficacy of aprotinin to improve anticoagulation, and to investigate whether the prolongation of CACT reflects true anticoagulation or is an in vitro artifact. To elucidate this antithrombotic effect of aprotinin, this study was done in patients prone to reduced intraoperative heparin sensitivity. ⋯ Aprotinin treatment in combination with heparin leads to less thrombin generation during CPB. Aprotinin has anticoagulant properties. Celite-activated ACT is reliable for monitoring anticoagulation in the presence of aprotinin, because the prolonged CACT in the aprotinin group reflects improved anticoagulation. Kaolin-activated ACT does not reflect this effect of aprotinin.