Lambert Gavin, Elam Mikael, Friberg Peter, Lundborg Christopher, Gao Sinsia, Bergquist Jonas, Nitescu Petre
Department of Clinical Physiology, Sahlgrenska Hospital, Göteborg, Sweden.
J Physiol. 2006 Jan 15;570(Pt 2):421-8. doi: 10.1113/jphysiol.2005.095562. Epub 2005 Oct 27.
Continuous intracisternal infusion of bupivacaine for the management of intractable pain of the head and neck is effective in controlling pain in this patient group. With the catheter tip being located at the height of the C1 vertebral body, autonomic regulatory information may also be influenced by the infusion of bupivacaine. By combining direct sampling of cerebrospinal fluid (CSF), via a percutaneously placed catheter in the cisterna magna, with a noradrenaline and adrenaline isotope dilution method for examining sympathetic and adrenal medullary activity, we were able to quantify the release of brain neurotransmitters and examine efferent sympathetic nervous outflow in patients following intracisternal administration of bupivacaine. Despite severe pain, sympathetic and adrenal medullary activities were well within normal range (4.2 +/- 0.6 and 0.7 +/- 0.2 nmol min(-1), respectively, mean +/-S.E.M.). Intracisternal bupivacaine administration caused an almost instantaneous elevation in mean arterial blood pressure, increasing by 17 +/- 7 mmHg after 10 min (P < 0.01). Heart rate increased in parallel (17 +/- 5 beats min(-1)), and these changes coincided with an increase in sympathetic nervous activity, peaking with an approximately 50% increase over resting level 10 min after injection (P < 0.01). CSF levels of GABA were reduced following bupivacaine (P < 0.05). CSF catecholamines and serotonin, and EEG, remained unaffected. These results show that acutely administered bupivacaine in the cisterna magna of chronic pain sufferers leads to an activation of the sympathetic nervous system. The results suggest that the haemodynamic consequences occur as a result of interference with the neuronal circuitry in the brainstem. Although these effects are transient, they warrant caution at the induction of intracisternal local anaesthesia.
持续脑池内注入布比卡因治疗头颈部顽固性疼痛对该患者群体的疼痛控制有效。当导管尖端位于C1椎体高度时,布比卡因的注入可能也会影响自主神经调节信息。通过经皮穿刺在枕大池放置导管直接采集脑脊液(CSF),并结合去甲肾上腺素和肾上腺素同位素稀释法检测交感神经和肾上腺髓质活性,我们能够量化脑内神经递质的释放,并检测布比卡因脑池内给药后患者的传出交感神经流出情况。尽管存在严重疼痛,但交感神经和肾上腺髓质活性仍在正常范围内(分别为4.2±0.6和0.7±0.2 nmol min⁻¹,均值±标准误)。脑池内注入布比卡因导致平均动脉血压几乎立即升高,10分钟后升高17±7 mmHg(P<0.01)。心率平行增加(17±5次/分钟),这些变化与交感神经活性增加一致,在注射后10分钟达到峰值,比静息水平增加约50%(P<0.01)。布比卡因给药后CSF中GABA水平降低(P<0.05)。CSF儿茶酚胺、5-羟色胺和脑电图均未受影响。这些结果表明,在慢性疼痛患者的枕大池急性注入布比卡因会导致交感神经系统激活。结果提示,血流动力学后果是由于脑干神经元回路受到干扰所致。尽管这些影响是短暂的,但在诱导脑池内局部麻醉时仍需谨慎。