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학술저널
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
수록면
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.

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