Oh W S
Pain Management Center, Department of Anesthesiology, Samsung Medical Center, SungKyunKwan University School of Medicine, Seoul, Korea.
Int J Tissue React. 2002;24(1):11-21.
To reduce surgical stress, fentanyl is frequently used for neurosurgical procedures in which focal and/or global ischemia may occur. However, the effect of fentanyl on cytokine levels during ischemia/reperfusion is still uncertain. The goal of this study was to evaluate the effect of fentanyl infusion on levels of the proinflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, during global cerebral ischemia/reperfusion in rats using the intracerebral microdialysis technique. Forty male Sprague-Dawley rats weighing 280-320 g were randomly assigned to each of four groups: group 1 (no fentanyl infusion and only ischemia/reperfusion); group 2 (1.5 ng/ml of fentanyl infusion during ischemia/reperfusion) and group 3 (3 ng/ml of fentanyl infusion during ischemia/reperfusion) (n=5 in each group). The rats were anesthetized with an intraperitoneal injection of pentobarbital (50 mg/kg). They were then intubated and ventilated with room air using an animal ventilator. A CMA-12 probe was inserted into the left hippocampal CA-1 region according to the guidelines. Artificial cerebrospinal fluid was run from the inserted microdialysis probe and infused with or without fentanyl at 3 microl/min using a microinjection syringe pump during ischemia/reperfusion. Ischemia was induced by clamping the carotid arteries. Hemorrhagic hypotension was induced for 17 min via the femoral artery, and reperfusion was accomplished by unclamping the sling and reinfusing the blood via the femoral artery. After 2 h of stabilization, the microdialysate was collected 10 times every 17 min, just before ischemia (control), after ischemia (I) and after reperfusion (R1-R8), and stored at -80 degrees C until analysis using high-performance liquid chromatography During global ischemia/reperfusion, TNF-alpha and IL-1beta significantly increased at reperfusion (R5) compared with the control value (p < 0.05). However, in both cases of fentanyl infusion, TNF-alpha and IL-1beta showed no increase compared with the control value. Fentanyl inhibited an increase of the proinflammatory cytokines, TNF-alpha and IL-1beta levels, during global cerebral ischemia/reperfusion in rats.
为减轻手术应激，芬太尼常用于可能发生局灶性和/或全脑缺血的神经外科手术。然而，芬太尼对缺血/再灌注期间细胞因子水平的影响仍不确定。本研究的目的是使用脑内微透析技术评估在大鼠全脑缺血/再灌注期间输注芬太尼对促炎细胞因子肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β水平的影响。将40只体重280 - 320 g的雄性Sprague-Dawley大鼠随机分为四组：第1组（不输注芬太尼，仅进行缺血/再灌注）；第2组（在缺血/再灌注期间输注1.5 ng/ml芬太尼）和第3组（在缺血/再灌注期间输注3 ng/ml芬太尼）（每组n = 5）。大鼠腹腔注射戊巴比妥（50 mg/kg）麻醉。然后插管并使用动物呼吸机用室内空气进行通气。根据指南将CMA-12探针插入左侧海马CA-1区。在缺血/再灌注期间，从插入的微透析探针中流出人工脑脊液，并使用微量注射泵以3 μl/min的速度输注或不输注芬太尼。通过夹闭颈动脉诱导缺血。通过股动脉诱导出血性低血压17分钟，通过松开吊带并经股动脉重新注入血液实现再灌注。稳定2小时后，在缺血前（对照）、缺血后（I）和再灌注后（R1 - R）每17分钟收集10次微透析液，并在-80℃保存，直至使用高效液相色谱法进行分析。在全脑缺血/再灌注期间，与对照值相比，再灌注时（R5）TNF-α和IL-1β显著升高（p < 0.05）。然而，在两种芬太尼输注情况下，与对照值相比，TNF-α和IL-1β均未升高。芬太尼在大鼠全脑缺血/再灌注期间抑制了促炎细胞因子TNF-α和IL-1β水平的升高。
