Norman J G, Fink G W
Department of Surgery, University of South Florida, Tampa 33612, USA.
Am Surg. 1997 Jan;63(1):75-80.
It has long been held that the acute-phase and neuroendocrine response to stress requires afferent neural input for its propagation. To further clarify the role of afferent neural impulses in this process and to determine the ability of epidural anesthesia to attenuate the normal perioperative stress response, 39 patients undergoing uncomplicated abdominal aortic replacement were randomized to receive either general anesthesia with postoperative patient-controlled intravenous morphine (n = 19) or combined regional/general anesthesia with intraoperative epidural catheter anesthesia using Bupivacaine to the T4 dermatome level followed by postoperative epidural morphine (n = 20). The stress response was quantitated by blinded measurement of baseline and postoperative (0, 12, 24, 48, and 72 hours) serum cortisol, epinephrine norepinephrine, total catecholamines, interleukin (IL)-1beta, IL-6, tumor necrosis factor (TNF)-alpha, and C-reactive protein (CRP). Total operative time (4.2 +/- 0.3 vs 4.3 +/- 0.4 hours), 72-hour fluid requirement (7.0 +/- 0.6 vs 6.8 +/- 0.71 mL), and length of hospitalization (7.8 +/- 1.4 vs 8.1 +/- 1.2 days) were not different between groups. All patients showed a significant increase in cortisol, epinephrine, norepinephrine, total catecholamines, CRP, and IL-6 in the postoperative period (P < 0.05). IL-1beta and TNF-alpha were less predictable and undetectable in most patients. There was no difference in any of the stress response indices between those patients receiving patient-controlled or epidural catheter anesthesia. In fact, the only parameter that was predictive of increased activation of the stress response was the length of operation, irrespective of anesthetic method. Those patients with operative times greater than 5 hours (n = 10) developed significantly higher CRP, IL-1beta, IL-6, and TNF-alpha levels (P < 0.05) at 12 and 24 hours postoperatively than those with total operative times less than 4 hours (n = 16). The neuroendocrine response to major surgical stress is propagated normally despite epidural blockade and is intensified with prolonged operative times. The inflammatory cytokines appear to play a major role in this process.
长期以来，人们一直认为，对压力的急性期和神经内分泌反应需要传入神经输入来进行传导。为了进一步阐明传入神经冲动在此过程中的作用，并确定硬膜外麻醉减弱围手术期正常应激反应的能力，将39例接受单纯腹主动脉置换术的患者随机分为两组，一组接受全身麻醉并术后患者自控静脉注射吗啡（n = 19），另一组接受区域/全身联合麻醉，术中使用布比卡因至T4皮节水平进行硬膜外导管麻醉，术后使用硬膜外吗啡（n = 20）。通过对基线及术后（0、12、24、48和72小时）血清皮质醇、肾上腺素、去甲肾上腺素、总儿茶酚胺、白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α和C反应蛋白（CRP）进行盲法测量来量化应激反应。两组患者的总手术时间（4.2±0.3 vs 4.3±0.4小时）、72小时液体需求量（7.0±0.6 vs 6.8±0.71 mL）和住院时间（7.8±1.4 vs 8.1±1.2天）无差异。所有患者术后皮质醇、肾上腺素、去甲肾上腺素、总儿茶酚胺、CRP和IL-6均显著升高（P < 0.05）。IL-1β和TNF-α的变化较难预测，大多数患者检测不到。接受患者自控麻醉或硬膜外导管麻醉的患者在任何应激反应指标上均无差异。事实上，唯一能预测应激反应激活增加的参数是手术时间，与麻醉方法无关。手术时间大于5小时的患者（n = 10）术后12小时和24小时的CRP、IL-1β、IL-6和TNF-α水平显著高于总手术时间小于4小时的患者（n = 16）（P < 0.05）。尽管有硬膜外阻滞，对重大手术应激的神经内分泌反应仍能正常传导，且随着手术时间延长而增强。炎症细胞因子似乎在这一过程中起主要作用。
