Activation of D1 Dopamine Receptors Induces Emergence from Isoflurane General Anesthesia.
Taylor NE, Chemali JJ, Brown EN, Solt K.
* Clinical Fellow, Department of Anaesthesia, Harvard Medical School, Boston, Massachusetts, and Resident, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts. ? Research Assistant, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital. ? Anesthetist, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital; Warren M. Zapol Professor, Department of Anaesthesia, Harvard Medical School; Professor of Computational Neuroscience, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts; Professor of Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology. § Assistant Professor, Department of Anaesthesia, Harvard Medical School; Assistant Anesthetist, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital; and Research Affiliate, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology.
Abstract
BACKGROUND: A recent study showed that methylphenidate induces emergence from isoflurane anesthesia. Methylphenidate inhibits dopamine and norepinephrine reuptake transporters. The objective of this study was to test the hypothesis that selective dopamine receptor activation induces emergence from isoflurane anesthesia.
METHODS: In adult rats, we tested the effects of chloro-APB (D1 agonist) and quinpirole (D2 agonist) on time to emergence from isoflurane general anesthesia. We then performed a dose-response study to test for chloro-APB-induced restoration of righting during continuous isoflurane anesthesia. SCH-23390 (D1 antagonist) was used to confirm that the effects induced by chloro-APB are specifically mediated by D1 receptors. In a separate group of animals, spectral analysis was performed on surface electroencephalogram recordings to assess neurophysiologic changes induced by chloro-APB and quinpirole during isoflurane general anesthesia.
RESULTS: Chloro-APB decreased median time to emergence from 330 to 50 s. The median difference in time to emergence between the saline control group (n = 6) and the chloro-APB group (n = 6) was 222 s (95% CI: 77-534 s, Mann-Whitney test). This difference was statistically significant (P = 0.0082). During continuous isoflurane anesthesia, chloro-APB dose-dependently restored righting (n = 6) and decreased electroencephalogram δ power (n = 4). These effects were inhibited by pretreatment with SCH-23390. Quinpirole did not restore righting (n = 6) and had no significant effect on the electroencephalogram (n = 4) during continuous isoflurane anesthesia.
CONCLUSIONS: Activation of D1 receptors by chloro-APB decreases time to emergence from isoflurane anesthesia and produces behavioral and neurophysiologic evidence of arousal during continuous isoflurane anesthesia. These findings suggest that selective activation of a D1 receptor-mediated arousal mechanism is sufficient to induce emergence from isoflurane general anesthesia.
Effects of Propofol, Sevoflurane, Remifentanil, and (S)-Ketamine in Subanesthetic Concentrations on Visceral and Somatosensory Pain-evoked Potentials.
Untergehrer G, Jordan D, Eyl S, Schneider G.
* Research Fellow, ‡ Professor, Director, and Chair, Department of Anesthesiology, Helios Clinic Wuppertal, Witten/Herdecke University, Wuppertal, Germany. † Research Fellow, Department of Anesthesiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Abstract
BACKGROUND: Although electroencephalographic parameters and auditory evoked potentials (AEP) reflect the hypnotic component of anesthesia, there is currently no specific and mechanism-based monitoring tool for anesthesia-induced blockade of nociceptive inputs. The aim of this study was to assess visceral pain-evoked potentials (VPEP) and contact heat-evoked potentials (CHEP) as electroencephalographic indicators of drug-induced changes of visceral and somatosensory pain. Additionally, AEP and electroencephalographic permutation entropy were used to evaluate sedative components of the applied drugs.
METHODS: In a study enrolling 60 volunteers, VPEP, CHEP (amplitude N2-P1), and AEP (latency Nb, amplitude Pa-Nb) were recorded without drug application and at two subanesthetic concentration levels of propofol, sevoflurane, remifentanil, or (s)-ketamine. Drug-induced changes of evoked potentials were analyzed. VPEP were generated by electric stimuli using bipolar electrodes positioned in the distal esophagus. For CHEP, heat pulses were given to the medial aspect of the right forearm using a CHEP stimulator. In addition to AEP, electroencephalographic permutation entropy was used to indicate level of sedation.
RESULTS: With increasing concentrations of propofol, sevoflurane, remifentanil, and (s)-ketamine, VPEP and CHEP N2-P1 amplitudes decreased. AEP and electroencephalographic permutation entropy showed neither clinically relevant nor statistically significant suppression of cortical activity during drug application.
CONCLUSIONS: Decreasing VPEP and CHEP amplitudes under subanesthetic concentrations of propofol, sevoflurane, remifentanil, and (s)-ketamine indicate suppressive drug effects. These effects seem to be specific for analgesia.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
亚麻醉浓度的丙泊酚、七氟烷、瑞芬太尼和盐酸Ketamine对内脏和躯体疼痛诱发电位的作用
【第347篇】乳腺癌手术后行切口及肋间神经罗哌卡因浸润在术后慢性疼痛中的作用:一项双盲随机临床试验 Anesthesiology. 118(2):318-326, February 2013.
A Double-blind Randomized Trial of Wound and Intercostal Space Infiltration with Ropivacaine during Breast Cancer Surgery: Effects on Chronic Postoperative Pain
Albi-Feldzer, Aline M.D.*; Mouret-Fourme E, Emmanuelle M.D.?; Hamouda, Smail M.D.?; Motamed, Cyrus M.D.§; Dubois, Pierre-Yves M.D.‖; Jouanneau, Ludivine Ph.D.?; Jayr, Christian M.D., Ph.D.*
Abstract
Background: The efficacy of local anesthetic wound infiltration for the treatment of acute and chronic postoperative pain is controversial and there are no detailed studies. The primary objective of this study was to evaluate the influence of ropivacaine wound infiltration on chronic pain after breast surgery.
Methods: In this prospective, randomized, double-blind, parallel-group, placebo-controlled study, 236 patients scheduled for breast cancer surgery were randomized (1:1) to receive ropivacaine or placebo infiltration of the wound, the second and third intercostal spaces and the humeral insertion of major pectoralis. Acute pain, analgesic consumption, nausea and vomiting were assessed every 30 min for 2 h in the postanesthesia care unit and every 6 h for 48 h. Chronic pain was evaluated 3 months, 6 months, and 1 yr after surgery by the brief pain inventory, hospital anxiety and depression, and neuropathic pain questionnaires.
Results: Ropivacaine wound infiltration significantly decreased immediate postoperative pain for the first 90 min, but did not decrease chronic pain at 3 months (primary endpoint), or at 6 and 12 months postoperatively. At 3 months, the incidence of chronic pain was 33% and 27% (P = 0.37) in the ropivacaine and placebo groups, respectively. During follow-up, brief pain inventory, neuropathic pain, and anxiety increased over time in both groups (P < 0.001) while depression remained stable. No complications occurred.
Conclusion: This multicenter, prospective study shows that ropivacaine wound infiltration after breast cancer surgery decreased immediate postoperative pain but did not decrease chronic pain at 3, 6, and 12 months postoperatively.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~