EFFECTS OF FENTANYL-LIDOCAINE-PROPOFOL AND DEXMEDETOMIDINE-LIDOCAINE-PROPOFOL ON TRACHEAL INTUBATION WITHOUT USE OF MUSCLE RELAXANTS Volkan Hancı, Gülay Erdoğan, Rahşan Dilek Okyay, Bülent Serhan Yurtlu, Hilal Ayoğlu, Yunus Baydilek, and Işıl Özkoçak Turan Department of Anesthesiology and Reanimation, School of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey.
The aim of this study was to compare the effects of fentanyl or dexmedetomidine when used in combination with propofol and lidocaine for tracheal intubation without using muscle relaxants. Sixty patients with American Society of Anesthesiologists stage I risk were randomized to receive 1 μg/kg dexmedetomidine (Group D, n = 30) or 2 μg/kg fentanyl (Group F, n = 30), both in combination with 1.5 mg/kg lidocaine and 3 mg/kg propofol. The requirement for intubation was determined based on mask ventilation capability, jaw motility, position of the vocal cords and the patient’s response to intubation and inflation of the endotracheal tube cuff. Systolic arterial pressure, mean arterial pressure, heart rate and peripheral oxygen saturation values were also recorded. Rate pressure products were calculated. Jaw relaxation, position of the vocal cords and patient’s response to intubation and inflation of the endotracheal tube cuff were significantly better in Group D than in Group F (p < 0.05). The intubation conditions were significantly more satisfactory in Group D than in Group F (p = 0.01). Heart rate was significantly lower in Group D than in Group F after the administration of the study drugs and intubation (p < 0.05). Mean arterial pressure was significantly lower in Group F than in Group D after propofol injection and at 3 and 5 minutes after intubation (p < 0.05). After intubation, the rate pressure product values were significantly lower in Group D than in Group F (p < 0.05). We conclude that endotracheal intubation was better with the dexmedetomidine–lidocaine–propofol combination than with the fentanyl–lidocaine–propofol combination. However, side effects such as bradycardia should be considered when using dexmedetomidine.
Key Words: dexmedetomidine, fentanyl, neuromuscular blocking agents, rate pressure products, tracheal intubation (Kaohsiung J Med Sci 2010;26:244–50)
Received: Mar 23, 2009 Accepted: Dec 15, 2009 Address correspondence and reprint requests to: Dr Volkan Hancı, Tepebaşı mahallesi, Yapkent sokak, Kale sitesi, A13 Blok, Daire 10, Zonguldak, Turkey. E-mail:
[email protected] or
[email protected]
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Muscle relaxants are frequently used to facilitate endotracheal intubation during the induction of anesthesia [1,2]. However, the administration of short-acting depolarizing muscle relaxants is associated with postoperative myalgias, malignant hyperthermia, hyperkalemia and increased intracranial or intraocular Kaohsiung J Med Sci May 2010 • Vol 26 • No 5 © 2010 Elsevier. All rights reserved.
Dexmedetomidine for tracheal intubation
pressure. The use of non-depolarizing muscle relaxants may cause prolonged neuromuscular blockade, potentiate histamine release, increase the risk of side effects associated with anticholinesterase-mediated reversal of these agents, and prevent rapid reversal of neuromuscular blockade in the event of an unexpected difficult intubation [1–6]. When the use of muscle relaxants is undesirable or contraindicated, the administration of correct induction agents to provide good intubating conditions without using muscle relaxants is an important consideration [1–5]. Dexmedetomidine is a highly selective α2 adrenoceptor agonist with analgesic and sedative effects, but it does not cause respiratory depression [7–9]. It is commonly used in the intensive care unit and is a well tolerated and acceptable sedative agent [7–9]. In combination with propofol, dexmedetomidine has been demonstrated to assist in extubation, fiberoptic intubation, awake blind nasotracheal intubation and laryngeal mask airway placement [7–14]. Although propofol with fentanyl, remifentanil alfentanil and lidocaine has successfully been used for endotracheal intubation without muscle relaxants [1–3,15,16], there is no information on dexmedetomidine in combination with propofol for laryngoscopic endotracheal intubation in the absence of muscle relaxants. Therefore, the aim of this study was to investigate the efficacy of dexmedetomidine-lidocaine-propofol compared with fentanyllidocaine-propofol for laryngoscopy and endotracheal intubation in the absence of muscle relaxants.
METHODS After approval of the hospital ethics committee and having informed consent from the patients, a total of 60 patients were enrolled in this study. All patients were
aged between 18–59 years, with American Society of Anesthesiologists stage I risk, and with no history of drug or alcohol abuse or cardiovascular and cerebrovascular diseases. The patients were hospitalized for elective surgery under general anesthesia and had difficult intubations. All patients were all Mallampati Class I and had a body mass index of < 30 kg/m2. The patients were randomized into two equal groups using a random samples table. Thirty minutes before induction, all patients were premedicated with an intramuscular injection of 0.07 mg/kg midazolam. In the operation room, a 20-G cannula was inserted for intravenous access, and 5–7 mL/kg of Ringer’s lactate solution was administered. The baseline arterial blood pressure, peripheral oxygen saturation, electrocardiogram and end-tidal CO2 measurements were obtained for all patients using standard monitoring equipment. Preoxygenation was performed for 3 minutes with 5 L/min of 100% oxygen. After preoxygenation, Group D received 1 μg/kg dexmedetomidine (100 μg/mL; Precedex, Hospira Inc., Lake Forest, IL, USA) diluted to a total volume of 10 mL and infused within 10 minutes using a calibrated electronic infusion pump (Braun Infusomat, Braun, Melsungen Germany) (Figure 1). Then, 5 mL of 0.9% saline was administered within 30 seconds. Group F received 10 mL of 0.9% saline infused within 10 minutes using a calibrated electronic infusion pump followed by 2 μg/kg fentanyl (50 μg/mL; Fentanyl Citrate, Hospira Inc.), which was diluted to a total volume of 5 mL and administered within 30 seconds. Immediately after administration of medications, all patients were given 1.5 mg/kg lidocaine, not to exceed a total of 100 mg per patient, followed by 3 mg/kg propofol over 30 seconds. After loss of consciousness, mask ventilation was initiated. Mask ventilation was 30 sec
30 min
3 min
60 sec Mask ventilation
10 min Intubation
Premedication
Preoxygenation Group D
Dexmedetomidine infusion Saline 0.9%
Group F
Saline 0.9% infusion
Fentanyl
Lidocaine
Propofol
Lidocaine
Propofol
Figure 1. Flow chart showing the time and duration of administration of each drug. Group D = dexmedetomidine–propofol–lidocaine group; Group F = fentanyl–propofol–lidocaine group. Kaohsiung J Med Sci May 2010 • Vol 26 • No 5
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assessed in all patients with a three-point scoring system (1 = adequate; 2 = difficult but possible; 3 = not possible). Mask ventilation was maintained for 60 seconds until intubation. For all patients, intubation was performed by the same anesthesiologist, who had not been informed of the drug being used. Intubation was performed using a Macintosh 3 laryngoscope blade and an 8.0-mm endotracheal tube for males and a 7.5-mm endotracheal tube for females. After tracheal intubation, the endotracheal tube cuff (ETTc) was gently inflated using an analog manometer (Cuff pressure gauge; VBM Medizintechnik, GmbH, Sulz, Germany) to between 20–25 cmH2O in all patients. The intubation conditions were assessed in all patients using a scoring system that included jaw relaxation (1 = fully relaxed; 2 = mild resistance; 3 = tight but open; 4 = impossible), vocal cord position (1 = wide open; 2 = mid-position; 3 = moving but open; 4 = closed), and response to intubation and inflation of the ETTc (1 = none; 2 = diaphragmatic movement; 3 = slight cough; 4 = severe cough) [15]. According to these criteria, intubation conditions were accepted as “excellent” in patients with a score of 3, “good” in patients with scores of 4–6, “bad” in those with scores of 7–9, and “inadequate” in those with scores of 10–12 [15]. Heart rate (HR), systolic arterial pressure (SAP), mean arterial pressure (MAP) and peripheral oxygen saturation were recorded for all patients at the following times: before induction, at drug administration, after propofol administration, at endotracheal intubation, and 3 and 5 minutes after intubation. The rate pressure product (RPP) was calculated for each time-point using the formula RPP = HR × SAP. If endotracheal intubation could not be successfully performed on the first attempt, patients received 0.6 mg/kg rocuronium. Atropine (0.5 mg) could be administered for bradycardia (HR < 50 beats/min). Ephedrine (5 mg) was administered if MAP decreased below 30% of the patient’s baseline control value for a minimum of 60 seconds. Complications during intubation such as coughing, laryngospasm, bronchospasm and muscle rigidity were also recorded. After intubation, anesthesia was maintained in all patients with 66% nitrous oxide in oxygen and 0.5% sevoflurane. Patients were ventilated to maintain end-tidal CO2 values of 35–40 mmHg. Painful surgical stimuli were avoided during the study. All data were analyzed using SPSS version 10.0 (SPSS Inc., Chicago, IL, USA). Descriptive statistics for 246
continuous variables are given as mean ± standard deviation. Categorical variables are shown as percentage. One-way analysis of variance was used to compare HR, blood pressure (MAP and SAP), peripheral oxygen saturation, age, height, weight, mean intubation condition score and intubation times. Intra-group analyses were conducted using t tests with repeated measurements. The χ2 test was used for sex, side effects, intubation condition scores and American Society of Anesthesiologists physical condition. Pearson’s correlation coefficients were determined to evaluate the correlation between intubation condition score and RPP value after intubation. Values of p < 0.05 were considered statistically significant. In a previous report using a combination of fentanyl and propofol for tracheal intubation without muscle relaxant, the incidence of poor and inadequate intubation condition was approximately 37.5% [16]. Based on these data, and to detect an absolute difference of 30% between the proportions of poor and inadequate intubating conditions with 80% power and a 0.05 level of significance, 23 patients were required in each group.
RESULTS There were no differences between the two groups in terms of demographic characteristics (Table 1). The HR was significantly different between the two groups after the administration of the study drugs (p < 0.001) and after intubation (p = 0.023), and was lower in Group D than in Group F. In Group D, the HR after dexmedetomidine administration and after propofol administration was significantly lower than the control values (p < 0.05). In Group F, the HR after propofol administration and at 3 and 5 minutes after
Table 1. Demographic characteristics of patients in this study* Group D (n = 30)
Group F (n = 30)
Age (yr) 35.77 ± 11.15 32.50 ± 10.75 Height (cm) 164.33 ± 6.99 167.60 ± 8.76 Weight (kg) 70.57 ± 12.18 69.37 ± 12.12 Sex, male/female 11/19 16/14
p 0.253 0.116 0.703 0.194
*Data presented as n or mean ± standard deviation. Group D = dexmedetomidine–propofol–lidocaine group; Group F = fentanyl–propofol–lidocaine group.
Kaohsiung J Med Sci May 2010 • Vol 26 • No 5
Dexmedetomidine for tracheal intubation B Group D Group F
Heart rate (beat/min)
90 *
85
‡
‡
80 75
‡
* †
70
†
65
105
Group D Group F
100 Mean arterial pressure (mmHg)
A
* †
95
*
90 ‡
85 ‡
80
‡
75
‡
70
60 Control
After D&F
After Propofol
Control
0 min 3 min 5 min After Intubation
* †
After D&F
After Propofol
0 min 3 min 5 min After Intubation
intubation was significantly lower than the control values (p < 0.05) (Figure 2). MAP after propofol administration and at 3 and 5 minutes after intubation was significantly lower in Group F than in Group D (p < 0.05). In Group D, the MAP after propofol and at 5 minutes after intubation was significantly lower than the control values (p < 0.05). In Group F, the MAP after propofol administration and at 3 and 5 minutes after intubation were significantly lower than the control values (p < 0.05) (Figure 2). The RRP values after the administration of the study drugs (p = 0.019) and after intubation (p = 0.036) were significantly lower in Group D than in Group F. In Group D, the RPP values after dexmedetomidine administration and after propofol administration, at intubation, and at 3 and 5 minutes after intubation were significantly lower than the control values (p < 0.05). In Group F, the RPP values after propofol administration and at 3 and 5 minutes after intubation were significantly lower than the control values (p < 0.05) (Figure 3). There were no statistically significant intergroup or intragroup differences in peripheral oxygen saturation measured at each time-point (p > 0.05). Six patients in Group D required atropine, versus none in Group F, which was statistically significant (p < 0.05). None of the patients in either group required ephedrine. When mask ventilation conditions before intubation were assessed, we found that three patients in Group F had difficulty in mask ventilation, while all patients in Group D had adequate mask ventilation. Kaohsiung J Med Sci May 2010 • Vol 26 • No 5
Rate pressure product (×1,000)
Figure 2. Changes in (A) heart rate and (B) mean arterial pressure after the administration of dexmedetomidine–propofol–lidocaine (Group D) or fentanyl–propofol–lidocaine (Group F). *p < 0.05 for Group D vs. Group F (one-way analysis of variance); †p < 0.05 for Group D vs. the control value (t test); ‡p < 0.05 for Group F vs. the control value (t test); After D&F = after dexmedetomidine and fentanyl administration; After propofol = after propofol administration.
11.5 11.0 10.5 10.0 9.5 9.0 8.5 8.0 7.5 7.0 6.5
Group D Group F
* *
† †
† † ‡
† ‡
Control
After D&F
After propofol
‡ 0 min 3 min 5 min After intubation
Figure 3. Changes in the rate pressure product after the administration of dexmedetomidine–propofol–lidocaine (Group D) or fentanyl–propofol–lidocaine (Group F). *p < 0.05 for Group D vs. Group F (one-way analysis of variance); †p < 0.05 for Group D vs. the control value (t test); ‡p < 0.05 for Group F vs. the control value (t test); After D&F = after dexmedetomidine and fentanyl administration; After propofol = after propofol administration.
This difference did not reach statistical significance (p > 0.05) (Table 2). Scores for jaw relaxation before intubation (p = 0.019), the position of the vocal cords during intubation (p = 0.035), and response to intubation and inflation of the ETTc (p = 0.039) were significantly better in Group D than in Group F. The overall intubation condition score based on all criteria was significantly better in Group D than in Group F (p = 0.010). The mean intubation condition score was also significantly lower in Group D than in Group F (p = 0.03) (Table 2). Pearson’s correlation analysis revealed a moderate positive correlation between the intubation condition 247
V. Hancı, G. Erdoğan, R.D. Okyay, et al Table 2. Intubation condition scores of patients* Group D (n = 30)
Group F (n = 30)
Mask ventilation Easy Difficult
30 (100) 0
27 (90.0) 3 (10.0)
Jaw relaxation Fully relaxed Mild resistance Tight but open
29 (96.7) 1 (3.3) 0
21 (70.0) 5 (16.7) 4 (13.3)
Vocal cord position Wide open Mid-position Moving but open
20 (66.7) 9 (30.0) 1 (3.3)
12 (40.0) 11 (36.7) 7 (23.3)
Response to intubation and ETTc None Diaphragmatic movement Slight cough Severe cough
17 (56.7) 4 (13.3) 7 (23.3) 2 (6.7)
10 (33.3) 4 (13.3) 5 (16.7) 11 (36.7)
Intubation condition score Excellent Good Poor Inadequate
17 (56.7) 11 (36.7) 2 (6.7) 0
9 (30.0) 8 (26.7) 9 (30.0) 4 (13.3)
4.20 ± 1.21
5.88 ± 2.44
Mean intubation condition score
p 0.237
0.019
0.035
0.039
0.010
0.030
*Data presented as n (%) or mean ± standard deviation. Group D = Dexmedetomidine–propofol–lidocaine group; Group F = fentanyl–propofol–lidocaine group; ETTc = endotracheal tube cuff.
score and the RPP value after intubation (p = 0.004, r = 0.375). None of the patients in either group required muscle relaxants for intubation. Furthermore, none of the patients had laryngospasm or bronchospasm. In Group F, muscle rigidity rendered mask ventilation difficult in three patients. However, there was no difference between the two groups in terms of the development of muscle rigidity (p > 0.05).
DISCUSSION Dexmedetomidine is a highly selective α2 adrenoceptor agonist with analgesic and sedative effects [7,8,12,14,17,18]. In this study, the administration of dexmedetomidine in combination with propofol and lidocaine provided better intubation conditions than with fentanyl. Propofol and lidocaine in combination with either dexmedetomidine or fentanyl blunt intubation-induced hemodynamic responses; however, MAP and RPP are more stable with dexmedetomidine 248
than with fentanyl. We demonstrated that the combination of dexmedetomidine, propofol and lidocaine is more suitable than the combination of fentanyl, propofol and lidocaine for tracheal intubation without using muscle relaxants. Dexmedetomidine was reported to blunt hemodynamic responses during laryngoscopy, intubation and extubation [19–22]. Snapir et al [23] reported that dexmedetomidine reduced myocardial perfusion, myocardial oxygen demand and the RPP. In this study, dexmedetomidine significantly reduced the RPP compared with the control value. In addition, the blunting effect on RPP responses during laryngoscopy was significantly better with dexmedetomidine than with fentanyl. Üzümcügil et al [9] compared dexmedetomidinepropofol and fentanyl-propofol combinations during laryngeal mask placement and concluded that dexmedetomidine is as successful as fentanyl in terms of mask placement conditions. Similarly, we found that intubation without muscle relaxants can be better achieved when dexmedetomidine, rather than fentanyl, is combined with a propofol–lidocaine regimen. Kaohsiung J Med Sci May 2010 • Vol 26 • No 5
Dexmedetomidine for tracheal intubation
Üzümcügil et al [9] also reported greater MAP decreases with fentanyl than with dexmedetomidine, although there was no significant difference between the two groups. It was reported that, after a dose of 2.0–2.5 mg/kg propofol, the mean blood pressure may decrease by 25–40% due to its vasodilatory and myocardial depressing effects [24]. Following a bolus dose of dexmedetomidine, an increase in blood pressure of 22% and a decrease in HR of 27% may occur due to its effects on peripheral α2 adrenoceptors [24]. We observed a smaller decrease in MAP in Group D, as compared with control values, than in Group F. We think that this is due to the effects of dexmedetomidine on peripheral α2 adrenoceptors. Although the decrease in MAP in Group F was well tolerated in these pre-hydrated, healthy young subjects, we believe this may constitute a risk for elderly, hypovolemic and debilitated patients. Üzümcügil et al [9] used fentanyl and dexmedetomidine in their similar study and reported that both drugs reduce HR. However, the decrease was not clinically significant. In our study, the mean HR was lower in Group D than in Group F, necessitating an increased use of atropine in Group D. We believe that this decrease in HR constitutes a risk for elderly patients and therefore warrants attention. Previous studies have demonstrated that a single 0.5 μg/kg dose of dexmedetomidine before extubation in pediatric patients blunted the airway reflexes and hemodynamic responses to extubation [25,26]. Similarly, in our study, diaphragmatic movements and coughing in response to intubation and inflation of the ETTc were significantly lower in Group D than in Group F. In vitro studies conducted on the bronchial tissue of human and animal subjects showed that α2 adrenoceptor stimulation can attenuate and prevent bronchoconstriction [27,28]. In an experimental study, 0.5 μg/kg of intravenous dexmedetomidine inhibited bronchoconstriction caused by histamine in dogs anesthetized with thiopental [29]. The authors of that study concluded that dexmedetomidine may be very useful in patients with high airway reactivity [29]. We think that dexmedetomidine can attenuate bronchial reactivity and airway reflexes, such as coughing, which can be an advantage in tracheal intubation without using muscle relaxants. To prevent hypertension, tachycardia and the development of the coughing reflex in response to laryngoscopy, we administered 1.5 mg/kg lidocaine to all Kaohsiung J Med Sci May 2010 • Vol 26 • No 5
patients before propofol administration [15,16]. Previous studies support the synergistic effect of lidocaine in combination with propofol [16,30]. Therefore, the synergistic effects of the lidocaine–propofol– dexmedetomidine combination may be among the factors responsible for the highly favorable intubation conditions in this study. Muscle rigidity is a common side effect of opioids after rapid injection and may interfere with mask ventilation [15]. In our study, although muscle rigidity occurred in three patients in Group F, it was not observed in Group D. We did not need to include a control group given with propofol alone because increasing the conventional induction dose of propofol might elicit adverse hemodynamic effects. In conclusion, our study has shown that in adult patients with normal airways 1 μg/kg dexmedetomidine before propofol and lidocaine induction provides better intubation conditions without muscle relaxants than 2 μg/kg fentanyl. Therefore, dexmedetomidine may offer an alternative to opioids in combination with propofol for intubation without muscle relaxants. However, side effects such as bradycardia should be considered when administering dexmedetomidine.
REFERENCES 1.
2.
3.
4.
5.
6.
7.
Stevens JB, Wheatley L. Tracheal intubation in ambulatory surgery patients: using remifentanil and propofol without muscle relaxants. Anesth Analg 1998;86:45–9. Erhan E, Ugur G, Gunusen I, et al. Propofol – not thiopental or etomidate – with remifentanil provides adequate intubating conditions in the absence of neuromuscular blockade. Can J Anaesth 2003;50:108–15. Collins L, Prentice J, Vaghadia H. Tracheal intubation of outpatients with and without muscle relaxants. Can J Anaesth 2000;47:427–32. Durmus M, Ender G, Kadir BA, et al. Remifentanil with thiopental for tracheal intubation without muscle relaxants. Anesth Analg 2003;96:1336–9. Stevens JB, Vescovo MV, Harris KC, et al. Tracheal intubation using alfentanil and no muscle relaxant: is the choice of hypnotic important? Anesth Analg 1997;84:1222–6. Shields JA. Heart block and prolonged Q-Tc interval following muscle relaxant reversal: a case report. AANA J 2008;76:41–5. Scher CS, Gitlin MC. Dexmedetomidine and low-dose ketamine provide adequate sedation for awake fibreoptic intubation. Can J Anaesth 2003;50:607–10.
249
V. Hancı, G. Erdoğan, R.D. Okyay, et al 8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
250
Jooste EH, Ohkawa S, Sun LS. Fiberoptic intubation with dexmedetomidine in two children with spinal cord impingements. Anesth Analg 2005;101:1248. Uzümcügil F, Canbay O, Celebi N, et al. Comparison of dexmedetomidine-propofol vs fentanyl-propofol for laryngeal mask insertion. Eur J Anaesthesiol 2008;25: 675–80. Avitsian R, Lin J, Lotto M, et al. Dexmedetomidine and awake fiberoptic intubation for possible cervical spine myelopathy: a clinical series. J Neurosurg Anesthesiol 2005;17:97–9. Grant SA, Breslin DS, MacLeod DB, et al. Dexmedetomidine infusion for sedation during fiberoptic intubation: a report of three cases. J Clin Anesth 2004; 16:124–6. Maroof M, Khan RM, Jain D, et al. Dexmedetomidine is a useful adjunct for awake intubation. Can J Anesth 2005;52:776–7. Nagashima M, Kunisawa T, Takahata O, et al. Dexmedetomidine infusion for sedation during awake intubation. Masui 2008;57:731–4. Abdelmalak B, Makary L, Hoban J, et al. Dexmedetomidine as sole sedative for awake intubation in management of the critical airway. J Clin Anesth 2007; 19:370–3. Jabbour-Khoury IS, Dabbous AS, Rizk LB, et al. A combination of alfentanil-lidocaine-propofol provides better intubating conditions than fentanyl-lidocaine-propofol in the absence of muscle relaxants. Can J Anaesth 2003; 50:116–20. Taha S, Siddik-Sayyid S, Alameddine M, et al. Propofol is superior to thiopental for intubation without muscle relaxants. Can J Anaesth 2005;52:249–53. Bergese SD, Khabiri B, Roberts WD, et al. Dexmedetomidine for conscious sedation in difficult awake fiberoptic intubation cases. J Clin Anesth 2007;19:141–4. Stamenkovic DM, Hassid M. Dexmedetomidine for fiberoptic intubation of a patient with severe mental retardation and atlantoaxial instability. Acta Anaesthesiol Scand 2006;50:1314–5. Yildiz M, Tavlan A, Tuncer S, et al. Effect of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation: perioperative haemodynamics and anaesthetic requirements. Drugs R D 2006;7:43–52.
20. Jaakola ML, Ali-Melkkilä T, Kanto J, et al. Dexmedetomidine reduces intraocular pressure, intubation responses and anaesthetic requirements in patients undergoing ophthalmic surgery. Br J Anaesth 1992;68: 570–5. 21. Scheinin B, Lindgren L, Randell T, et al. Dexmedetomidine attenuates sympathoadrenal responses to tracheal intubation and reduces the need for thiopentone and peroperative fentanyl. Br J Anaesth 1992;68:126–31. 22. Lawrence CJ, Lange S. Effects of a single pre-operative dexmedetomidine dose on isoflurane requirements and peri-operative hemodynamic stability. Anaesthesia 1997;52:736–4. 23. Snapir A, Posti J, Kentala E, et al. Effects of low and high plasma concentrations of dexmedetomidine on myocardial perfusion and cardiac function in healthy male subjects. Anesthesiology 2006;105:902–10. 24. Reves JG, Glass PSA, Lubarsky DA, et al. Intravenous nonopioid anesthetics. In: Miller RD, ed. Miller’s Anesthesia, 6th edition. Philadelphia: Elsevier Churchill Livingstone, 2005:317–79. 25. Guler G, Akin A, Tosun Z, et al. Single-dose dexmedetomidine reduces agitation and provides smooth extubation after pediatric adenotonsillectomy. Paediatr Anaesth 2005;15:762–6. 26. Guler G, Akin A, Tosun Z, et al. Single-dose dexmedetomidine attenuates airway and circulatory reflexes during extubation. Acta Anaesthesiol Scand 2005;49:1088–91. 27. Grundström N, Andersson RGG, Wikberg JES. Prejunctional alpha2 adrenoceptors inhibit contraction of tracheal smooth muscle by inhibiting cholinergic neurotransmission. Life Sci 1981;28:2981–6 28. Lou YP, Franco-Cereceda A, Lundberg JM. Variable alpha2-adrenoceptor mediated inhibition of bronchoconstriction and peptide release upon activation of pulmonary afferents. Eur J Pharmacol 1992; 210: 173–81. 29. Groeben H, Mitzner W, Brown RH. Effects of the alpha2adrenoceptor agonist dexmedetomidine on bronchoconstriction in dogs. Anesthesiology 2004;100:359–63. 30. Woods AW, Grant S, Harten J, et al. Tracheal intubating conditions after induction with propofol, remifentanil and lignocaine. Eur J Anaesthesiol 1998;15:714–8.
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