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      Does a single dose of intravenous nicardipine or nimodipine affect the bispectral index following rapid sequence intubation?

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          Abstract

          Background

          Theoretically, L-type calcium channel blockers could modulate anesthetic effects. Nicardipine does not affect the bispectral index (BIS), but nimodipine, which can penetrate the blood-brain barrier, has not been studied. The aim of this study was to evaluate whether a single dose of intravenous nicardipine or nimodipine could affect BIS following rapid sequence intubation.

          Methods

          This study was done in a double-blind, randomized fashion. Anesthesia was induced with fentanyl 2 µg/kg, thiopental sodium 5 mg/kg, and 100% oxygen. After loss of consciousness, patients received rocuronium 1.0 mg/kg and either a bolus of 20 µg/kg nicardipine, nimodipine, or a comparable volume of normal saline (n = 20). Intubation was performed 1 min after study drug administration. BIS, mean blood pressure (MBP), and heart rate (HR) were measured before anesthetic induction, after loss of consciousness, before intubation, during intubation, and 1, 2 and 5 min after intubation.

          Results

          BIS dropped rapidly after induction but increased to 60 before intubation in all groups irrespective of study drug. In nimodipine, the increase in BIS during intubation was not significant compared to pre-intubation, in contrast to the other two groups, but there was no difference in BIS during intubation. HR significantly increased, but MBP just rose to pre-induction values after intubation in nicardipine and nimodipine groups. BIS, MBP, and HR following intubation increased in control group.

          Conclusions

          A single dose of intravenous nicardipine or nimodipine could attenuate blood pressure increases but not affect BIS increases in rapid sequence intubation.

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          Most cited references28

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          Potentiation of antinociceptive effects of morphine by calcium-channel blockers at the level of the spinal cord.

          Opioids inhibit voltage-dependent calcium-channel conductance, which is essential for the nervous system to be able to signal a painful event. Accordingly, interference with calcium-channel conductance may enhance opioid analgesia. The current study was designed to investigate the effects of calcium-channel blocking drugs on the antinociception of morphine at the level of the spinal cord. Rats were chronically implanted with catheters in the lumbar intrathecal space. Tail-flick test was used to assess thermal nociception. Intrathecally administered drugs were morphine, calcium-channel blockers (verapamil, diltiazem, and nicardipine), or a combination of morphine and calcium-channel blocker. Intrathecal administration of morphine produced a significant dose-dependent antinociception in the tail-flick test. In contrast, intrathecal administration of calcium-channel blockers, verapamil, diltiazem, and nicardipine, did not show any antinociception at the employed doses. However, when intrathecally administered calcium-channel blockers, verapamil (50 micrograms), diltiazem (100 micrograms), or nicardipine (20 micrograms), were combined with ineffective (0.25, 0.5, 1, or 2 micrograms) or moderately effective (5 micrograms) doses of intrathecally administered morphine, significant antinociception was produced. These interactions were synergistic. There were no significant changes in MAP or HR after the intrathecal administration of 200 micrograms verapamil or 2 micrograms morphine combined with 50 micrograms verapamil. The authors interpreted these results to indicate that calcium-channel blocking drugs synergistically potentiate the analgesic effects of morphine at the level of the spinal cord. Before these results can be translated into clinical use, however, adequate toxicity studies must be conducted to examine the effect of the perispinal administration of calcium-channel blocking drugs on spinal cord function.
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            Effects of dose-dependent levels of isoflurane on cerebral blood flow in healthy subjects studied using positron emission tomography.

            In this study, we tested the hypothesis that escalating drug concentrations of isoflurane are associated with a significant decline in cerebral blood flow (CBF) in regions sub-serving conscious brain activity, including specifically the thalamus. Nine human volunteers received three escalating drug concentrations: 0.2, 0.4 and 1.0 MAC end-tidal inhalation. During waking, baseline and the three levels of sedation, aO PET scan was performed. Isoflurane decreased the bispectral index (BIS) values dose-dependently. Cardiovascular and respiratory parameters were maintained constant over time. No significant change in global CBF was observed. Throughout all three MAC levels of sedation, isoflurane caused an increased regional cerebral blood flow (rCBF) in the anterior cingulate and decreased rCBF in the cerebellum. Initially, isoflurane (0 vs. 0.2 MAC) significantly increased relative rCBF in the medial frontal gyrus and in the nucleus accumbens. At the next level (0.2 vs. 0.4 MAC), relative rCBF was significantly increased in the caudate nucleus and decreased in the lingual gyrus and cuneus. At the last level (0.4 vs. 1 MAC), relative rCBF was significantly increased in the insula and decreased in the thalamus, the cuneus and lingual gyrus. Compared with flow distribution in awake volunteers, 1 MAC of isoflurane significantly raised relative activity in the anterior cingulate and insula regions. In contrast, a significant relative flow reduction was identified in the thalamus, the cerebellum and lingual gyrus. Isoflurane, like sevoflurane, induced characteristic flow redistribution at doses of 0.2-1.0 MAC. At 1 MAC of isoflurane, rCBF decreased in the thalamus. Specific areas affected by both isoflurane and sevoflurane included the anterior cingulate, insula regions, cerebellum, lingual gyrus and thalamus.
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              Which is responsible for the haemodynamic response due to laryngoscopy and endotracheal intubation? Catecholamines, vasopressin or angiotensin?

              We have investigated the concentrations of epinephrine, norepinephrine, vasopressin and angiotensin converting enzyme activity to explore the role of these mediators in the neuroendocrine response to laryngoscopy and tracheal intubation. One hundred (50 male, 50 female) ASA I patients aged 20-50 yr (mean+/-SEM; 35.59+/-0.99) were included in the study. They were undergoing elective surgery under standard anaesthesia induction and maintenance using tracheal intubation. Plasma concentrations of epinephrine, norepinephrine and vasopressin as well as plasma angiotensin converting enzyme activity were determined at four time points, before (T1) and after (T2) induction, and 2 (T3) and 5 min (T4) after intubation. Blood pressure and heart rate were recorded at corresponding times to reveal if any correlation existed between haemodynamic parameters and neuroendocrine response. Heart rate increased after induction and intubation (P<0.05) and decreased significantly at T4 (P<0.05). Systolic blood pressure decreased significantly (P<0.05) after induction and increased slightly after intubation decreasing to below baseline value (P<0.05) at T4. Diastolic blood pressure increased slightly after intubation and decreased significantly (P<0.05) at T4. Plasma epinephrine and norepinephrine concentrations decreased after induction and increased at T3 and T4 without reaching significance. Vasopressin concentrations increased slightly at T2 and T3 and decreased significantly at T4 (P<0.05). Angiotensin converting enzyme activity was unaffected when compared with baseline values. Blood pressure, heart rate, plasma epinephrine, norepinephrine and vasopressin concentrations increased slightly in response to laryngoscopy and intubation, all returning to or below baseline 5 min later with no change in angiotensin converting enzyme activity in normotensive patients.
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                Author and article information

                Journal
                Korean J Anesthesiol
                KJAE
                Korean Journal of Anesthesiology
                The Korean Society of Anesthesiologists
                2005-6419
                2005-7563
                October 2010
                21 October 2010
                : 59
                : 4
                : 256-259
                Affiliations
                Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
                Author notes
                Corresponding author: Jie Ae Kim, M.D., Ph.D., Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50, Ilwon-dong, Kangnam-gu, Seoul 135-710, Korea. Tel: 82-2-3410-0363, Fax: 82-2-3410-6626, jakim0813@ 123456yahoo.com
                Article
                10.4097/kjae.2010.59.4.256
                2966706
                21057615
                21bb15fc-7894-401b-950f-8a495a3e4527
                Copyright © The Korean Society of Anesthesiologists, 2010

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 04 March 2010
                : 01 June 2010
                : 14 June 2010
                Categories
                Clinical Research Article

                Anesthesiology & Pain management
                nimodipine,nicardipine,intubation,bis
                Anesthesiology & Pain management
                nimodipine, nicardipine, intubation, bis

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