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      KCI등재 SCOPUS SCIE

      Propofol 마취하에서 기관내삽관과 Desflurane의 흡입에 의한 심박수 및 혈압 상승 효과의 비교 = Comparison of the effects on increase of heart rate and blood pressure between tracheal intubation and desflurane inhalation during propofol anesthesia

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      https://www.riss.kr/link?id=A104356669

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      다국어 초록 (Multilingual Abstract)

      Background: This study was undertaken to compare the hemodynamic effects between desflurane inhalation and endotracheal intubation, and to evaluate the intensity of airway irritation by desflurane inhalation of high concentration.
      Methods: Twenty adult patients with ASA 1 were enrolled in this study. Radial artery was catheterized and heart rate (HR) and mean arterial pressure (MAP) were measured throughout the study. Anesthesia was induced by propofol and effect site concentration of propofol was maintained at 4μg/ml using target controlled infusor (TCI). Peak HR and MAP following tracheal intubation were recorded and inhalation of 12 vol% desflurane was started after HR and MAP had been returned to pre-intubation value. The HR, MAP, inspiratory (Fi) and end-tidal fraction (Et) were observed after desflurane inhalation for 10 minutes.
      Results: The HR and MAP were significantly increased after tracheal intubation and desflurane inhalation, and the peak hemodynamic change after desflurane inhalation was significantly delayed as compared to tracheal intubation. The maximal HR change from baseline after tracheal intubation or desflurane inhalation was not different, but maximal MAP change was significantly lower during desflurane inhalation compared with tracheal intubation. The maximal change of HR and MAP when end-tidal fraction of desflurane had been reached 6 vol% was lower than that of tracheal intubation or desflurane inhalation.
      Conclusions: Despite of propofol administration required for general anesthesia, the HR and MAP were significantly increased during desflurane inhalation of high concentration. In particular, the extent of HR increase during desflurane inhalation was similar to that by tracheal intubation. (Korean J Anesthesiol 2006; 50: 25~9)
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      Background: This study was undertaken to compare the hemodynamic effects between desflurane inhalation and endotracheal intubation, and to evaluate the intensity of airway irritation by desflurane inhalation of high concentration. Methods: Twenty...

      Background: This study was undertaken to compare the hemodynamic effects between desflurane inhalation and endotracheal intubation, and to evaluate the intensity of airway irritation by desflurane inhalation of high concentration.
      Methods: Twenty adult patients with ASA 1 were enrolled in this study. Radial artery was catheterized and heart rate (HR) and mean arterial pressure (MAP) were measured throughout the study. Anesthesia was induced by propofol and effect site concentration of propofol was maintained at 4μg/ml using target controlled infusor (TCI). Peak HR and MAP following tracheal intubation were recorded and inhalation of 12 vol% desflurane was started after HR and MAP had been returned to pre-intubation value. The HR, MAP, inspiratory (Fi) and end-tidal fraction (Et) were observed after desflurane inhalation for 10 minutes.
      Results: The HR and MAP were significantly increased after tracheal intubation and desflurane inhalation, and the peak hemodynamic change after desflurane inhalation was significantly delayed as compared to tracheal intubation. The maximal HR change from baseline after tracheal intubation or desflurane inhalation was not different, but maximal MAP change was significantly lower during desflurane inhalation compared with tracheal intubation. The maximal change of HR and MAP when end-tidal fraction of desflurane had been reached 6 vol% was lower than that of tracheal intubation or desflurane inhalation.
      Conclusions: Despite of propofol administration required for general anesthesia, the HR and MAP were significantly increased during desflurane inhalation of high concentration. In particular, the extent of HR increase during desflurane inhalation was similar to that by tracheal intubation. (Korean J Anesthesiol 2006; 50: 25~9)

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      참고문헌 (Reference)

      1 DeSouza GJ, "Which is most pungent: isoflurane, sevoflurane or desflurane?" 85 : 305-307, 2000

      2 Eger EI II, "Uptake and distribution" Churchill Livingstone 74-95, 2000

      3 Gonsowski CT, "Toxicity of compound A in rats.Effect of increasing duration of administration" 80 : 566-73, 1994

      4 Helman JD, "The risk of myocardial ischemia in patients receiving desflurane versus sufentanil anesthesia for coronary artery bypass graft surgery" 47-62, anesthesiology1992

      5 Eger EI 2nd, "The effect of anesthetic duration on kinetic and recovery characteristics of desflurane versus sevoflurane,and on the kinetic characteristics of compound A,in volunteers" 86 : 414-421, 1998

      6 Ebert TJ, "Sympathetic responses to induction of anesthesia in humans with propofol or etomidate" 76 : 725-33, 1992

      7 Ebert TJ, "Sympathetic hyperactivity during desflurane anesthesia in healthy volunteers" 79 : 444-53, 1993

      8 Ciofolo MJ, "Sympathetic activation by desflurane is not mediated by airway or lung receptors" A218. -, 1995

      9 Weiskopf RB, "Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans" 80 : 1035-45, 1994

      10 Moore MA, "Rapid 1% increases of end-tidal desflurane concentration to greater than 5% transiently increase heart rate and blood pressure in humans" 81 : 94-8, 1994

      1 DeSouza GJ, "Which is most pungent: isoflurane, sevoflurane or desflurane?" 85 : 305-307, 2000

      2 Eger EI II, "Uptake and distribution" Churchill Livingstone 74-95, 2000

      3 Gonsowski CT, "Toxicity of compound A in rats.Effect of increasing duration of administration" 80 : 566-73, 1994

      4 Helman JD, "The risk of myocardial ischemia in patients receiving desflurane versus sufentanil anesthesia for coronary artery bypass graft surgery" 47-62, anesthesiology1992

      5 Eger EI 2nd, "The effect of anesthetic duration on kinetic and recovery characteristics of desflurane versus sevoflurane,and on the kinetic characteristics of compound A,in volunteers" 86 : 414-421, 1998

      6 Ebert TJ, "Sympathetic responses to induction of anesthesia in humans with propofol or etomidate" 76 : 725-33, 1992

      7 Ebert TJ, "Sympathetic hyperactivity during desflurane anesthesia in healthy volunteers" 79 : 444-53, 1993

      8 Ciofolo MJ, "Sympathetic activation by desflurane is not mediated by airway or lung receptors" A218. -, 1995

      9 Weiskopf RB, "Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans" 80 : 1035-45, 1994

      10 Moore MA, "Rapid 1% increases of end-tidal desflurane concentration to greater than 5% transiently increase heart rate and blood pressure in humans" 81 : 94-8, 1994

      11 Daniel M, "Propofol fails to attenuate the cardiovascular response to rapid increases in desflurane concentration" 84 : 75-80, 1996

      12 Muzi M, "Lidocaine airway anesthesia does not attenuate sympathetic activation during desflurane administration in humans" 81 : 1994

      13 Yasuda N, "Kinetics of desflurane,isoflurane,and halothane in humans" 74 : 489-98, 1991

      14 Gormley WP, "Intravenous lidocaine does not attenuate the cardiovascular and catecholamine response to a rapid increase in desflurane concentration" 82 : 358-361, 1996

      15 Ebert TJ, "Inhibition of sympathetic neural outflow during thiopental anesthesia in humans" 71 : 319-326, 1990

      16 Wrigley SR, "Induction and recovery characteristics of desflurane in day case patients:a comparison with propofol" 46 : 615-22, 1991

      17 Sutton TS, "Fluoride metabolites after prolonged exposure of volunteers and patients to desflurane" 73 : 180-5, 1991

      18 Weiskopf RB, "Fentanyl,esmolol,and clonidine blunt the transient cardiovascular stimulation induced by desflurane in humans" 81 : 1350-5, 1994

      19 Rodig G, "Effects of rapid increases of desflurane and sevoflurane to concentrations of 1.5 MAC on systemic vascular resistance and catecholamine response during cardiopulmonary bypass" 87 : 801-807, 1997

      20 Weiskopf RB, "Desflurane does not produce hepatic or renal injury in human volunteers" 74 : 570-4, 1992

      21 Bailey JM, "Context-sensitive half-times and other decrement times of inhaled anesthetics" 85 : 681-686, 1997

      22 Yasuda N, "Comparison of kinetics of sevoflurane and isoflurane in humans" 72 : 316-24, 1991

      23 Parsons RS, "Comparison of desflurane and fentanyl-based anaesthetic techniques for coronary artery bypass surgery" 72 : 430-, 1994

      24 Kharasch ED, "Clinical sevoflurane metabolism and disposition. I. Sevoflurane and metabolite pharmacokinetics" 82 : 1369-1378, 1995

      25 Holaday DA, "Clinical characteristics and biotransformation of sevoflurane in healthy human volunteers" 54 : 100-6, 1981

      26 Grundmann U, "Cardiovascular effects of desflurane and isoflurane in patients with coronary artery disease" 40 : 1101-1107, 1996

      27 Jones RM, "Biotransformation and hepato-renal function in volunteers after exposure to desflurane(I-653)" 64 : 482-7, 1990

      28 Yonker-Sell AE, "Alfentanil modifies the neurocirculatory responses to desflurane" 82 : 162-166, 1996

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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.09 0.09 0.1
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
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