Gilron I, Quirion R, Coderre T J
National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
Anesth Analg. 1999 Feb;88(2):414-20. doi: 10.1097/00000539-199902000-00036.
We evaluated the suppression of spinal Fos-like immunoreactivity (FLI) by i.v. anesthetics in the rat formalin model. Preformalin injection (1.5% subcutaneously) treatment groups included i.v. saline controls and three i.v. GABAergic anesthetic groups (pentobarbital 20 mg/kg, propofol 10 mg/kg, or alphaxalone 1.5 mg/kg; n = 12 per group). After perfusion 2 h postformalin, spinal cords were dissected, sliced at 30 microm, and processed by immunoperoxidase staining with an antibody against the Fos protein. Quantification and determination of the laminar distribution of Fos-labeled nuclei were performed at the L4-5 spinal level ipsilateral to formalin injection. Drug groups demonstrating FLI suppression were comparatively studied in a 5-min postformalin treatment group. Pentobarbital pretreatment failed to suppress FLI. However, significant reductions (percent decrease) of FLI were observed with propofol (63%) and alphaxalone (30%) compared with saline controls. Pre- versus postformalin comparison studies showed that propofol, but not alphaxalone, suppressed FLI more effectively when given preformalin. Given the observed inconsistencies between this study of Fos expression and our previous behavioral study, it is questionable whether anesthetic modulation of noxious stimulus-induced FLI parallels that of behavioral responses.
In this study, we examined whether i.v. general anesthetics (propofol, alphaxalone, and pentobarbital) prevent injury-induced spinal cord changes. We measured spinal Fos protein after rats received anesthetics before versus after a formalin injection. Fos inhibition patterns were inconsistent with behavioral studies of these anesthetics, suggesting that Fos inhibition does not always correlate with behavioral analgesia.
我们在大鼠福尔马林模型中评估了静脉麻醉药对脊髓Fos样免疫反应性（FLI）的抑制作用。福尔马林注射前（皮下注射1.5%）治疗组包括静脉注射生理盐水对照组和三个静脉注射GABA能麻醉药组（戊巴比妥20mg/kg、丙泊酚10mg/kg或alphaxalone 1.5mg/kg；每组n = 12）。福尔马林注射2小时后灌注，取出脊髓，切成30微米薄片，用抗Fos蛋白抗体进行免疫过氧化物酶染色处理。在福尔马林注射同侧的L4 - 5脊髓水平进行Fos标记细胞核的层状分布定量和测定。在福尔马林注射后5分钟的治疗组中对显示出FLI抑制作用的药物组进行了比较研究。戊巴比妥预处理未能抑制FLI。然而，与生理盐水对照组相比，丙泊酚（63%）和alphaxalone（30%）观察到FLI显著降低（降低百分比）。福尔马林注射前后的比较研究表明，福尔马林注射前给予丙泊酚比alphaxalone更有效地抑制FLI。鉴于本研究中Fos表达与我们之前行为学研究之间观察到的不一致性，有害刺激诱导的FLI的麻醉调节是否与行为反应的麻醉调节平行尚值得怀疑。
在本研究中，我们研究了静脉全身麻醉药（丙泊酚、alphaxalone和戊巴比妥）是否能预防损伤诱导的脊髓变化。我们在大鼠接受福尔马林注射前后给予麻醉药后测量脊髓Fos蛋白。Fos抑制模式与这些麻醉药的行为学研究不一致，表明Fos抑制并不总是与行为性镇痛相关。
