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首页> 外文期刊>The Internet Journal of Neuromonitoring >Dexmedetomidine Effects on Brain Tissue Oxygenation Measured by Frequency Domain Near Infrared Spectroscopy
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Dexmedetomidine Effects on Brain Tissue Oxygenation Measured by Frequency Domain Near Infrared Spectroscopy

机译：用频域近红外光谱法测定右美托咪定对脑组织氧合的影响

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摘要

Dexmedetomidine (DEX) is a selective alpha2-adrenergic agonist that produces cerebral vasoconstriction. We used frequency domain near infrared spectroscopy (FD-NIRS) to study brain oxygenation during DEX intravenous bolus injection. Oxyhemoglobin (OHb), deoxyhemoglobin (HHb), brain oxygen saturation (SO2) and total hemoglobin (tHb) were acquired on the frontal right and left side in 4 neurosurgery patients without cerebral pathology. Measurements were performed using a portable brain oxymeter, Oxiplex TS (ISS, Champaign, IL). Dexmedetomidine 0.2 mcg/kg was given to attenuate hypertension during the initial stages of desflurane anesthesia. During DEX administration, regional cerebral OHb decreased from 17.7 ± 6.9 ?Mol/L to 16.1 ± 6.3 ?Mol/L (p < 0.05) and SO2 from 61 ± 12 % to 58 ± 12 % (p < 0.05). HHb did not change from 10.5 ± 2.8 ?Mol to 10.5 ± 2.7 ?Mol/L. Recovery of brain oxygenation to pre-DEX levels occurred within 5 minutes. After administration of DEX, a small but consistent decrease in OHb was observed, probably mediated by a local vasoconstrictor effect. Brain oxygenation decreased transiently with DEX treatment without an increase in HHb production. Introduction Dexmedetomidine (DEX) is a selective alpha2-adrenergic agonist with sedative and analgesic effects [1,2]. DEX enhances anesthesia produced by other anesthetic drugs and decreases blood pressure by stimulating central alpha2 and imidazoline receptors [3,4]. The use of DEX in neuroanesthesia generate a reduction in the sympathetic tone and a decrease in peripheral noradrenaline release reducing hypertensive responses to neurosurgical patient stimulation during catheterization and head pin holder application. However, initially direct activation of cerebral α2b receptors produces local vasoconstriction effect that leads to a transient increase in arterial blood pressure and a decrease in cerebral blood flow [5,6]. A common problem during neurosurgical procedures is the interference of anesthetic drug during intraoperative action potential recording. DEX has been used as an elective anesthetic drug in awake craniotomy during resection of brain lesions in eloquent areas in order to decrease anesthetic use without attenuating neuronal function [7]. Procedures performed with intraoperative feedback from the patient reduced the morbidity associated with surgical treatment of critical brain areas. A rapid restoration in the level of consciousness in the postoperative period without respiratory depression and significant cognitive impairment has popularized the use of this drug in intensive care units [2].In previous studies, a neuroprotective mechanism has been described with the use of DEX [8], that may be related to a reduction in the release of catecholamine during cerebral hypoxic-ischemia [9]. However, this may conflict with other reports that DEX produces direct cerebral vasoconstriction and may decrease brain oxygen delivery[10]. Quantitative brain tissue oxygenation monitoring has been established in animals using frequency domain near infrared spectrometry method (FD-NIRS) [11], and more recently in clinical studies [12]. As opposed to continuous wave methods of brain tissue oxygenation monitoring, FD-NIRS utilizes spatially resolved frequency domain information to measure absolute absorption and scattering of near infra-red light and calculate absolute concentrations of oxyhemoglobin (OHb) and deoxyhemoglobin (HHb) in brain tissue. The purpose of this investigation was to determine if brain oxygenation decreased during the initial period of DEX bolus treatment in relation to cerebral vasoconstriction. Methods Clinical protocol: Four patients who underwent neurosurgery were enrolled on this initial study. Surgeries included spinal cord or peripheral nerve procedures. Institutional review approval from the University of Illinois at Chicago was obtained for this study. Written informed consent was obtained from all subjects prior to participation in this study
机译：右美托咪定（DEX）是产生脑血管收缩的选择性α2-肾上腺素能激动剂。我们使用频域近红外光谱（FD-NIRS）研究DEX静脉推注期间的脑氧合。在4例无脑病理的神经外科患者中，在额叶右侧和左侧采集了氧合血红蛋白（OHb），脱氧血红蛋白（HHb），脑血氧饱和度（SO2）和总血红蛋白（tHb）。使用便携式脑血氧仪Oxiplex TS（ISS，Champaign，IL）进行测量。在地氟醚麻醉的初始阶段，给予右旋美托咪定0.2 mcg / kg以减轻高血压。在DEX给药期间，局部脑OHb从17.7±6.9？Mol / L降至16.1±6.3？Mol / L（p <0.05），而SO2从61±12％降至58±12％（p <0.05）。 HHb从10.5±2.8 µMol / L不变。 5分钟内大脑氧合恢复到DEX之前的水平。服用DEX后，观察到OHb少量但持续下降，可能是由局部血管收缩作用介导的。用DEX进行治疗时，脑部的氧合暂时减少，而HHb的产生却没有增加。简介右美托咪定（DEX）是一种具有镇静和镇痛作用的选择性α2-肾上腺素能激动剂[1,2]。 DEX通过刺激中枢α2和咪唑啉受体来增强其他麻醉药产生的麻醉作用并降低血压[3,4]。在神经麻醉中使用DEX可以减少交感神经张力，减少周围的去甲肾上腺素释放，从而减少在导管插入术和头部固定器应用过程中对神经外科患者刺激产生的高血压反应。然而，最初直接激活脑α2b受体会产生局部血管收缩作用，从而导致动脉血压短暂升高和脑血流量降低[5,6]。神经外科手术过程中的一个普遍问题是术中动作电位记录过程中麻醉药物的干扰。 DEX在清醒性开颅手术中在雄辩区域的脑部病变切除术中已用作选择性麻醉药，目的是减少麻醉药的使用而不削弱神经元功能[7]。在患者术中反馈的情况下进行的手术减少了与关键脑区域的手术治疗相关的发病率。术后无呼吸抑制和明显的认知障碍的意识水平的快速恢复已在重症监护病房中广泛使用该药物[2]。在以前的研究中，已经描述了使用DEX来描述神经保护机制[ [8]，这可能与减少脑缺氧缺血过程中儿茶酚胺的释放有关[9]。但是，这可能与其他有关DEX产生直接的脑血管收缩并可能减少脑氧输送的报道相矛盾[10]。已经使用频域近红外光谱法（FD-NIRS）在动物中建立了定量的脑组织氧合监测[11]，最近在临床研究中[12]。与连续波方法进行脑组织氧合监测不同，FD-NIRS利用空间分辨的频域信息来测量近红外光的绝对吸收和散射，并计算脑组织中氧合血红蛋白（OHb）和脱氧血红蛋白（HHb）的绝对浓度。这项研究的目的是确定在与脑血管收缩有关的DEX推注治疗初期脑部氧合是否减少。方法临床规程：4例接受神经外科手术的患者入选了该初始研究。手术包括脊髓或周围神经手术。这项研究获得了芝加哥伊利诺伊大学的机构审查批准。在参与本研究之前，已从所有受试者获得书面知情同意

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