Kenichi Masui

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PURPOSE Temporary brain ischemia occurring during surgery under general anesthesia may induce the death of neuronal cells and cause severe neurological deficits. On the other hand, it is not clear whether μ-opioid receptor agonists promote ischemic brain injury. It is known that duration of ischemic depolarization affects the degree of neuronal damage.(More)
We measured the plasma levels of adrenomedullin (AM), a novel vasodilating peptide, in 89 patients with various forms of systemic inflammatory response syndrome (SIRS) and 13 healthy volunteers serving as controls. Plasma levels of AM in SIRS (burns: 20.5 +/- 3. 2 fmol/ml [mean +/- SEM]; pancreatitis: 13.8 +/- 3.8 fmol/ml; trauma: 14.9 +/- 2.5 fmol/ml;(More)
BACKGROUND With the growing use of pharmacokinetic (PK)-driven drug delivery and/or drug advisory displays, identifying the PK model that best characterizes propofol plasma concentration (Cp) across a variety of dosing conditions would be useful. We tested the accuracy of 3 compartmental models and 1 physiologically based recirculatory PK model for propofol(More)
Sympathetic activation after subarachnoid hemorrhage (SAH) can induce tachycardia as well as cardiac and brain injury. We examined the effects of beta1 receptor antagonist landiolol on hemodynamics and the levels of tissue injury markers in patients with SAH. Fifty-six SAH patients undergoing intracranial aneurysm surgery with tachycardia (>or=90 beats per(More)
Remifentanil has short half-lives: the values of alpha and beta decay are about 2 and 15 min, respectively. Therefore, the time for remifentanil concentration to reach its steady state concentration (Css) is shorter than those of other anesthetic drugs such as propofol and fentanyl. The Css and the time course of plasma concentration as well as effect-site(More)
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