Kunisawa T, Nagata O, Nagashima M, Mitamura S, Ueno M, Suzuki A, Takahata O, Iwasaki H: Dexmedetomidine suppresses the decrease in blood pressure during anesthetic induction and blunts the cardiovascular response to tracheal intubation

Department of Anesthesiology, Asahikawa Medical College, Asahikawa, Hokkaido, Japan.
Journal of clinical anesthesia (Impact Factor: 1.19). 06/2009; 21(3):194-9. DOI: 10.1016/j.jclinane.2008.08.015
Source: PubMed


To evaluate the effect of dexmedetomidine combined with fentanyl on hemodynamics.
Prospective, double-blinded, randomized study.
Operating room of a university hospital.
30 ASA physical status II and III patients with mild-to-moderate cardiovascular disease.
Patients were assigned to one of three groups: Group D-F2 [dexmedetomidine, effect-site concentration (ESC) of fentanyl = two ng/mL]; Group F2 (placebo, ESC of fentanyl = two ng/mL), or Group F4 (placebo, ESC of fentanyl = 4 ng/mL).
Dexmedetomidine (an initial dose of 1.0 microg/kg for 10 min, followed by a continuous infusion of 0.7 microg x kg(-1) x hr(-1)) or placebo saline was administered 15 minutes before anesthetic induction. Anesthesia was induced with propofol and fentanyl using a target-controlled infusion system. Hemodynamic parameters: systolic (SBP) and diastolic blood pressures (DBP), and heart rate (HR) during anesthetic induction were measured and the percent changes were calculated for both induction and intubation.
After inducing anesthesia, SBP was significantly higher in Group D-F2 (127 +/- 24 mmHg) than Group F2 (90 +/- 20 mmHg) or Group F4 (77 +/- 21 mmHg). The SBP in Groups F2 and F4 reached 160 +/- 31 mmHg and 123 +/- 36 mmHg, respectively, after intubation, but no significant change in SBP was noted in Group D-F2. The percent increase in SBP due to tracheal intubation in Group D-F2 was 3% +/- 4% and was significantly lower than that of Group F2 (70% +/- 34%) or Group F4 (45% +/- 36%).
Dexmedetomidine combined with fentanyl during anesthetic induction suppresses the decrease in blood pressure due to anesthetic induction and also blunts the cardiovascular response to tracheal intubation.

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    • "Kunisawa et al. [24] reported that an injection of dexmedetomidine inhibits a decrease in blood pressure caused by the anesthetics, and so postulated that it may be the result of vasoconstriction caused by the alpha-2 receptor in the vascular smooth muscle. The report stated that blood pressure temporarily increases one minute after an injection with a loading dose of dexmedetomidine, and reaches its peak at 3 min. "
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    ABSTRACT: This study was designed to compare the effect of dexmedetomidine and remifentanil used in anesthetic induction on hemodynamic change after direct laryngoscopy and tracheal intubation. A total of 90 ASA class 1 or 2 patients were randomly assigned to one of 3 groups to receive one of the following treatments in a double-blind manner: normal saline (Group C, n = 30), dexmedetomidine 1 µg/kg (Group D, n = 30), remifentanil 1 µg/kg (Group R, n= 30). Anesthesia was induced with propofol 2 mg/kg and rocuronium 0.6 mg/kg and maintained with 2 vol% sevoflurane and 50% nitrous oxide in oxygen. In group D, dexmedetomidine 1 µg/kg was infused for 10 min before tracheal intubation. Patients in group R was received 1 µg/kg of remifentanil 1 minute before tracheal intubation. The systolic blood pressure, diastolic blood pressure and heart rate were recorded from entrance to operation room to 5 min after tracheal intubation. The percent increase in systolic and diastolic blood pressure due to tracheal intubation in group D and R were significantly lower than that of group C (P < 0.05). The heart rate 1 min after tracheal intubation was lower in groups R and D than in the group C (P < 0.05). In healthy normotensive patients, the use of dexmedetomidine during anesthetic induction suppressed a decrease in blood pressure due to anesthetic induction and blunted the hemodynamic responses to endotracheal intubation.
    Korean journal of anesthesiology 08/2012; 63(2):124-9. DOI:10.4097/kjae.2012.63.2.124
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    • "A limitation of this study was that a dose-response experiment was not performed to determine the optimal dose of DEX that produces the maximum depression of FIC without causing side effects. However, our choice of doses was based on the DEX dose used in premedication (27). DEX is used as a premedicant in doses of 0.5 to 1 μg/kg because of its sedative and anesthetic-sparing effects, as well as attenuating airway/circulatory reflexes during anesthesia (11). "
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    ABSTRACT: The incidence of fentanyl-induced cough (FIC) during induction of general anesthesia varies around 40% and is undesirable. It increases intracranial, intraocular, and intra-abdominal pressures. This prospective, randomized, double-blind, placebo-controlled study evaluated the effect of dexmedetomidine (DEX) pretreatment on the incidence and severity of FIC. Altogether 300 patients undergoing elective surgical procedures were randomly allocated into three groups (I, II, III; n = 100) and administered intravenously, over 10 min, 10 mL isotonic saline, DEX 0.5 μg/kg in 10 mL isotonic saline, or DEX 1 μg/kg in 10 mL isotonic saline, respectively. All groups subsequently received a fentanyl (4.0 μg/kg) intravenous push. The incidence and severity of cough were recorded for 1 min after fentanyl administration. The incidence of FIC was 61%, 40%, and 18% in groups I, II, and III, respectively (P < 0.05 for treatment groups II and III versus control group I). There was no significant difference in the severity or onset time of cough, or hemodynamic variables, among the three groups. . Intravenous DEX (0.5 μg/kg or 1 μg/kg) immediately before the administration of intravenous fentanyl (4.0 μg/kg) significantly reduced the incidence of FIC.
    Upsala journal of medical sciences 03/2012; 117(1):18-21. DOI:10.3109/03009734.2011.629749 · 1.98 Impact Factor
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    • "Dexmedetomidine was administered intravenously using a target-controlled infusion technique. Although this technique has been reported for the administration of dexmedetomidine to human patients (Fragen & Fitzgerald, 1999; Tanskanen et al., 2006; Hammer et al., 2009; Kunisawa et al., 2009, 2010; Tsai et al., 2010), it is not representative of current clinical veterinary practice. In this study, target-controlled infusions were used in order to rapidly establish and maintain stable plasma concentrations . "
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    ABSTRACT: Escobar, A., Pypendop, B. H., Siao, K. T., Stanley, S. D., Ilkiw, J. E. Effect of dexmedetomidine on the minimum alveolar concentration of isoflurane in cats. J. vet. Pharmacol. Therap. 35, 163–168. This study reports the effects of dexmedetomidine on the minimum alveolar concentration of isoflurane (MACiso) in cats. Six healthy adult female cats were used. MACiso and dexmedetomidine pharmacokinetics had previously been determined in each individual. Cats were anesthetized with isoflurane in oxygen. Dexmedetomidine was administered intravenously using target-controlled infusions to maintain plasma concentrations of 0.16, 0.31, 0.63, 1.25, 2.5, 5, 10, and 20 ng/mL. MACiso was determined in triplicate at each target plasma dexmedetomidine concentration. Blood samples were collected and analyzed for dexmedetomidine concentration. The following model was fitted to the concentration–effect data: where MACiso.c is MACiso at plasma dexmedetomidine concentration C, MACiso.0 is MACiso in the absence of dexmedetomidine, Imax is the maximum possible reduction in MACiso, and IC50 is the plasma dexmedetomidine concentration producing 50% of Imax. Mean ± SE MACiso.0, determined in a previous study conducted under conditions identical to those in this study, was 2.07 ± 0.04. Weighted mean ± SE Imax, and IC50 estimated by the model were 1.76 ± 0.07%, and 1.05 ± 0.08 ng/mL, respectively. Dexmedetomidine decreased MACiso in a concentration-dependent manner. The lowest MACiso predicted by the model was 0.38 ± 0.08%, illustrating that dexmedetomidine alone is not expected to result in immobility in response to noxious stimulation in cats at any plasma concentration.
    Journal of Veterinary Pharmacology and Therapeutics 04/2011; 35(2):163-8. DOI:10.1111/j.1365-2885.2011.01301.x · 1.19 Impact Factor
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