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논문 기본 정보

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저자정보
Sanuki, Takuro (Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences) Mishima, Gaku (Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences) Kurata, Shinji (Department of Dental Anesthesiology, Nagasaki University Hospital) Watanabe, Toshihiro (Department of Dental Anesthesiology, Nagasaki University Hospital) Kiriishi, Kensuke (Department of Dental Anesthesiology, Nagasaki University Hospital) Tachi, Mizuki (Department of Dental Anesthesiology, Nagasaki University Hospital) Ozaki, Yu (Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences) Okayasu, Ichiro (Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences) Kawai, Mari (Division of Clinical Physiology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences) Matsushita, Yuki (Division of Clinical Oral On) Miura, Keiichiro Ayuse, Takao
저널정보
대한치과마취과학회 Journal of dental anesthesia and pain medicine Journal of dental anesthesia and pain medicine 제15권 제3호
발행연도
2015.1
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129 - 134 (6page)

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Background: We hypothesized that ketamine, when administered as the anesthetic induction agent, may prevent cardiovascular depression during high-dose remifentanil administration, unlike propofol. To test our hypothesis, we retrospectively compared the hemodynamic effects of ketamine, during high-dose remifentanil administration, with those of propofol. Methods: Thirty-eight patients who underwent oral surgery at the Nagasaki University Hospital between April 2014 and June 2015 were included in this study. Anesthesia was induced by the following procedure: First, high-dose remifentanil ($0.3-0.5{\mu}g/kg/min$) was administered 2-3 min before anesthesia induction;next, the anesthetic induction agent, either propofol (Group P) or ketamine (Group K), was administered. Mean arterial pressure (MAP) and the heart rate were recorded by the automated anesthesia recording system at four time points: immediately before the administration of high-dose remifentanil (T1);immediately before the administration of propofol or ketamine (T2);2.5 min (T3), and 5 min (T4) after the administration of the anesthetic induction agent. Results: In Group P, the MAP at T3 ($75.7{\pm}15.5mmHg$, P = 0.0015) and T4 ($68.3{\pm}12.5mmHg$, P < 0.001) were significantly lower than those at T1 ($94.0{\pm}12.4mmHg$). However, the MAP values in the K group were very similar (P = 0.133) at all time points. The heart rates in both Groups P (P = 0.254) and K (P = 0.859) remained unchanged over time. Conclusions: We showed that ketamine, when administered as the anesthetic induction agent during high-dose remifentanil administration, prevents cardiovascular depression.
#Hemodynamic changes #High-dose remifentanil anesthesia #Ketamine #Propofol

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참고문헌 (8)

참고문헌 신청
Kurata Y / 2008 / High-dose remifentanil anesthesia / J Clin Anesth 32:1692~1696 google schola Albertin A / 2005 / The effect-site concentration of remifentanil blunting cardiovascular responses to tracheal intubation and skin incision during bispectral index-guided propofol anesthesia / Anesth Analg 101:125~130 google schola Kortelainen J / 2009 / Effects of remifentanil on the spectrum and quantitative parameters of electroencephalogram in propofol anesthesia / Anesthesiology 111:574~583 google schola Tweed WA / 1972 / Circulatory responses to ketamine anesthesia / Anesthesiology 37:613~619 google schola Haas DA / 1992 / Ketamine: a review of its pharmacologic properties and use in ambulatory anesthesia / Anesth Prog 3:61~68 google schola

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