【精华】Anesthesiology，A&A 摘要翻译

GoalYou

【第365篇】多巴胺D1受体活化促进异氟烷全身麻醉苏醒 Anesthesiology.2013 Jan;118(1):30-39.

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.

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多巴胺D1受体活化促进异氟烷全身麻醉苏醒

背景：最近的一项研究表明哌醋甲酯促进异氟烷全身麻醉苏醒。哌醋甲酯能够抑制多巴胺和去甲肾上腺素的再摄取。本研究旨在验证选择性活化多巴胺受体可促进异氟烷全身麻醉苏醒的假说。

方法：在成年大鼠中，我们检测多巴胺D1受体激动剂（chloro-APB）和D2受体激动剂（quinpirole）对异氟烷全身麻醉苏醒时间的影响。然后，我们对chloro-APB促进持续异氟烷全身麻醉大鼠翻正反射恢复的作用进行剂量相关性研究。D1受体抑制剂（SCH-23390）用于证实chloro-APB通过选择性作用于D1受体发挥促进苏醒的作用。在单独一组动物中，我们对记录到的脑电图进行频谱分析，进而评价在持续异氟烷全身麻醉时chloro-APB和quinpirole对神经生理学影响。

结果：chloro-APB将苏醒中位时间从330s降低到50s。生理盐水组（n=6）和chloro-APB组（n=6）苏醒时间差值的中位数为222s（95% 可信区间: 77-534 s, Mann-Whitney test）。差异具有统计学意义（p=0.0082）。在异氟烷持续麻醉时，chloro-APB剂量依赖性促进翻正反射恢复（n=6）和减少δ 脑电波的活动（n=4）。通过SCH-23390预处理可抑制该作用。在异氟烷持续麻醉时，Quinpirole组未出现翻正反射恢复（n=6）及对脑电图无明显影响（n=4）。

结论：D1受体活化减少异氟烷全身麻醉的苏醒时间，觉醒行为学和神经生理学的证据明其在异氟烷持续全身麻醉时能够促进觉醒。这些发现提示，选择性激活D1受体足以导致异氟烷全身麻醉的苏醒。

solobruce

受益匪浅，希望继续能拜读到其他文章。

wuxing9915037

让我们的思路更加开阔

猫耳朵duo

非常感谢，能不能多传一些啊？

tt2sw2013

太厉害了:loveliness:

wuxing9915037

新进展，新收获，有利以后科研;P

sd667355

多谢分享，收益颇多

甜甜777

不错，认真学习中:victory:

小诺

好厉害呀，我要认真学习。:victory:

GoalYou

【第346篇】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Anesthesiology. 2013 Feb;118(2):308-17.

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.
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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

【摘要】

背景： 尽管脑电图和听觉诱发电位可反应麻醉的镇静作用，然而，目前没有特殊设备监测麻醉阻断伤害性刺激传入的情况。本研究旨在研究内脏痛诱发电位（VPEP）和热接触痛诱发电位（CHEP），如同脑电图一样，作为评价药物导致内脏和躯体疼痛改变的指标。此外，AEP和脑电图用于评估所研究药物的镇静作用。

方法： 该研究纳入60名自愿者，记录没有药物作用以及两组亚麻醉剂量丙泊酚、七氟烷、瑞芬太尼和盐酸Ketamine作用下的VPEP、CHEP和AEP。VPEP通过食管远端的双极电极产生。CHEP通过CHEP刺激器给予前臂中部热脉冲刺激产生。AEP和脑电图用于评价镇静情况。

结果： 随着丙泊酚、七氟烷、瑞芬太尼和盐酸Ketamine浓度升高，VPEP和CHEP N2-P1幅度振幅降低。AEP和脑电图结果表明药物作用未导致出现临床相关和有统计学意义差异的皮质活动度降低。

结论： 亚麻醉浓度的丙泊酚、七氟烷、瑞芬太尼和盐酸Ketamine导致VPEP和CHEP下降反应了药物的抑制作用。这些作用主要表现在镇痛方面。

GoalYou

【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.
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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

【摘要】

背景： 切口行局麻药浸润用于治疗术后急慢性疼痛的作用仍存在争议，而且目前没有具体的研究。该研究的主要目的是评价罗哌卡因切口局部浸润用于乳腺癌术后慢性疼痛的作用。

方法： 本研究为前瞻、随机、双盲、平行组设计、安慰剂对照的临床试验，236为拟行乳腺癌手术的患者随机分为两组，在切口局部，第二、三肋间隙以及胸大肌的肱骨连接处分别接受罗哌卡因或者安慰剂浸润。在麻醉恢复室的2小时内，每30分钟评估急性疼痛，镇痛药的使用量、恶心和呕吐情况，随后48小时内每6小时再次评估上述情况。术后3个月、6个月、1年通过简易疼痛量表、医院焦虑、抑郁以及神经病理性疼痛问卷评价慢性疼痛情况。

结果： 罗哌卡因切口浸润显著降低术后90分钟内的急性疼痛，但并未减轻术后3个月、6个月及12个月的慢性疼痛。在术后3个月时，罗哌卡因组和安慰剂组慢性疼痛的发生率分别为33%和27%（P = 0.37）。在随访期间，两组简易疼痛量表评分及神经病理痛、焦虑情况随着时间推移均升高（P < 0.001），然而抑郁情况相对稳定。没有并发症发生。

结论： 该多中心前瞻性研究表明乳腺癌术后罗哌卡因切口浸润减轻术后即刻疼痛，但无法减轻术后3个月、6个月、1年疼痛。

GoalYou

【第348篇】有关新鲜冰冻血浆/红细胞比值在产后大出血中作用的观察性研究 Anesth Analg. 2013 Jan;116(1):155-61.

An observational study of the fresh frozen plasma: red blood cell ratio in postpartum hemorrhage.

Pasquier P, Gayat E, Rackelboom T, La Rosa J, Tashkandi A, Tesniere A, Ravinet J, Vincent JL, Tsatsaris V, Ozier Y, Goffinet F, Mignon A.

Bégin Military Teaching Hospital, 69 avenue de Paris 94163 Saint-Mandé Cedex, France. pasquier9606@yahoo.f.

Abstract

BACKGROUND: Postpartum hemorrhage is the leading cause of maternal death worldwide. Recent data from trauma patients and patients with hemorrhagic shock have suggested that an increased fresh frozen plasma:red blood cell (FFP:RBC) ratio may be of benefit in massive bleeding. We addressed this issue in cases of severe postpartum hemorrhage.

METHODS: We reviewed data from all patients diagnosed with severe postpartum hemorrhage during a 4-year period (2006-2009). Patients who were treated with sulprostone and required transfusion within 6 hours of delivery were included in the study and were divided into 2 groups according to their response to sulprostone: bleeding controlled with sulprostone alone (sulprostone group) and bleeding requiring an additional advanced interventional procedure including arterial angiographic embolization and/or surgical procedures (arterial ligation, B-Lynch suture, or hysterectomy; intervention group). The requirement or no requirement for advanced procedures constituted the primary end point of the study. Propensity scoring was used to assess the effect of a high FFP:RBC ratio on bleeding control.

RESULTS: Among 12,226 deliveries during the study period, 142 (1.1%) were complicated by severe postpartum hemorrhage. Bleeding was controlled with sulprostone alone in 90 patients (63%). Advanced interventional procedures were required for 52 patients (37%). Forty-one patients were transfused with both RBCs and FFP. The FFP:RBC ratio increased over the study period (P < 0.001), from 1:1.8 at the start to 1:1.1 at the end of the study period. After propensity score modeling (inverse probability of treatment weighting), a high FFP:RBC ratio was associated with lower odds for advanced interventional procedures (odds ratio [95% confidence interval], 1.25 [1.07-1.47]; P = 0.008). There were no deaths, severe organ dysfunction, or other complications as a consequence of severe postpartum hemorrhage.

CONCLUSIONS: In this retrospective study, a higher FFP:RBC ratio was associated with a lower requirement for advanced interventional procedures in the setting of postpartum hemorrhage. The benefits of transfusion using a higher FFP:RBC ratio should be confirmed by randomized-controlled trials.
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有关新鲜冰冻血浆/红细胞比值在产后大出血中作用的观察性研究

摘要

背景： 在世界范围内，产后大出血均是产妇死亡最主要的原因。最近有关创伤患者和失血性休克患者的研究结果表明提高新鲜冰冻血浆：红细胞比率可能对大出血患者有利。我们对产后严重出血的情况进行相关研究。

方法： 我们回顾4年内（2006年-2009年）所有被诊断为严重产后出血患者的数据。患者产后6小时内需要噻普酮治疗和需要输血的患者纳入研究，并且根据其对噻普酮的反应分为两组：单独噻普酮可控制的出血（噻普酮组）和需要动脉血管栓塞和/或手术（动脉结扎、B-lynch缝扎术或子宫切除术）等进一步干预措施治疗的患者（干预组）。是否需要进一步干预作为该研究最主要的研究终点。倾向评分用于评价高FFP:RBC比值在控制出血中的作用。

结果： 研究期间共有12226产妇分娩，142例（1.1%）出现严重产后出血并发症。90位患者通过单独应用噻普酮可控制出血（63%）。52位患者需要进一步措施进行干预（37%）。41位患者同时输注红细胞和新鲜冰冻血浆。在研究过程期间，FFP:RBC的比值从开始的1:1.8上升到1:1.1。进行倾向评分建模（逆处理概率加权法）后发现，高FFP:RBC比值患者需要进一步干预治疗的风险小 (OR [95% CI], 1.25 [1.07-1.47]; P = 0.008)。严重产后出血未出现死亡，严重器官功能障碍或者其它并发症。

结论： 在该回顾性研究中，在产后大出血情况下，高FFP:RBC比值患者需要进一步干预治疗的风险小。以高FFP:RBC比值方式输注血制品的益处需要RCT研究进行确认。

GoalYou

【第349篇】发育早期暴露于挥发性麻醉药导致秀丽隐杆线虫行为缺陷 Anesth Analg. 2013 Jan;116(1):185-9.

Early Developmental Exposure to Volatile Anesthetics Causes Behavioral Defects in Caenorhabditis elegans.

Gentry KR, Steele LM, Sedensky MM, Morgan PG.

Department of Anesthesiology and Pain Medicine, Seattle Children's Hospital, M/S W 9824, PO Box 5371, Seattle, WA 98105. katherine.gentry@seattlechildrens.or.

Abstract

BACKGROUND: Mounting evidence from animal studies shows that anesthetic exposure in early life leads to apoptosis in the developing nervous system. This loss of neurons has functional consequences in adulthood. Clinical retrospective reviews have suggested that multiple anesthetic exposures in early childhood are associated with learning disabilities later in life as well. Despite much concern about this phenomenon, little is known about the mechanism by which anesthetics initiate neuronal cell death. Caenorhabditis elegans, a powerful genetic animal model, with precisely characterized neural development and cell death pathways, affords an excellent opportunity to study anesthetic-induced neurotoxicity. We hypothesized that exposing the nematode to volatile anesthetics early in life would induce neuron cell death, producing a behavioral defect that would be manifested in adulthood.

METHODS: After synchronization and hatching, larval worms were exposed to volatile anesthetics at their 95% effective concentration for 4 hours. On day 4 of life, exposed and control worms were tested for their ability to sense and move to an attractant (i.e., to chemotax). We determined the rate of successful chemotaxis using a standardized chemotaxis index.

RESULTS: Wild-type nematodes demonstrated striking deficits in chemotaxis indices after exposure to isoflurane (ISO) or sevoflurane (SEVO) in the first larval stage (chemotaxis index: untreated, 85 ± 2; ISO, 52 ± 2; SEVO, 47 ± 2; P < 0.05 for both exposures). The mitochondrial mutant gas-1 had a heightened effect from the anesthetic exposure (chemotaxis index: untreated, 71 ± 2; ISO, 29 ± 12; SEVO, 24 ± 13; P < 0.05 for both exposures). In contrast, animals unable to undergo apoptosis because of a mutation in the pathway that mediates programmed cell death (ced-3) retained their ability to sense and move toward an attractant (chemotaxis index: untreated, 76 ± 10; ISO, 73 ± 9; SEVO, 76 ± 10). Furthermore, we discovered that the window of greatest susceptibility to anesthetic neurotoxicity in nematodes occurs in the first larval stage after hatching (L1). This coincides with a period of neurogenesis in this model. All values are means ± SD.

CONCLUSION: These data indicate that anesthetics affect neurobehavior in nematodes, extending the range of phyla in which early exposure to volatile anesthetics has been shown to cause functional neurological deficits. This implies that anesthetic-induced neurotoxicity occurs via an ancient underlying mechanism. C elegans is a tractable model organism with which to survey an entire genome for molecules that mediate the toxic effects of volatile anesthetics on the developing nervous system.
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发育早期暴露于挥发性麻醉药导致秀丽隐杆线虫行为缺陷

背景： 众多动物研究的证据表明，生命早期暴露于麻醉药物可导致发育过程神经元凋亡。这些神经元丢失可导致成年后功能异常。回顾性临床研究表明儿童早期多次暴露于麻醉药物与其随后的学习障碍相关。尽管该现象得到众多关注，但是人们对麻醉药物导致神经元死亡的机制却知之甚少。秀丽隐杆线虫是一种很好的基因动物模型，其神经系统发育和细胞死亡通路具有明确的特征，为研究麻醉药物的神经毒性提供良好的机遇。我们假设线虫在生命早期暴露于挥发性气体可引起神经元死亡，导致成年后表现出行为异常。

方法： 在同步化孵化后，幼虫暴露于95%有效浓度的挥发性麻醉药物中4小时。在生命周期的第4天，检测暴露组和对照组对引诱剂的感知和运动能力（例如，趋化作用）。我们通过标准趋化指数来评价成功趋化的比例。

结果： 野生型线虫在幼虫第1阶段暴露于异氟烷（ISO）或七氟烷（SEVO）后导致显著的趋化障碍（趋化指数：未暴露，85 ± 2；ISO, 52 ± 2；SEVO， 47 ± 2；异氟烷和七氟烷组P值均小于0.05）。线粒体gas-1基因突变对麻醉药物暴露效应具有显著作用（趋化指数：未暴露，71 ± 2；ISO，29 ± 12；SEVO， 24 ± 13；异氟烷和七氟烷组P值均小于0.05）。相反，由于介导细胞程序死亡通路发生突变可使其保留对引诱剂的感知和运动能力感知和运动，因此动物不会发生神经元凋亡(趋化指数: 未暴露, 76 ± 10；ISO， 73 ± 9；SEVO，76 ± 10)。而且，我们发现线虫对麻醉药物最敏感的时间段是孵化后第1个幼虫期。这与该模型神经发育的时间相一致。所有结果有均数± 标准差表示。

结论： 这些结果表明麻醉药物能够影响线虫的神经行为，扩大了麻醉药物早期暴露导致神经功能异常的动物类属。这表明麻醉药物的神经毒性通过古老存在的机制发挥作用。秀丽隐杆线虫是一个容易处理的动物模型，可用于研究挥发性麻醉药对发育中神经系统毒性作用完整基因分子机制。