Sympathetic overactivity in active ulcerative colitis: effects of clonidine
Sympathetic overactivity in active ulcerative colitis: effects of clonidine
复制标题
DOI：
10.1152/ajpregu.00442.2005
复制
发表时间：
2006-01-01
影响因子：
2.8
通讯作者：
Malliani, A
中科院分区：
文献类型：
--
作者：
Furlan, R;Ardizzone, S;Malliani, A
以前的报告表明炎症性肠病可能伴随着神经自主神经的异常。我们验证了以下假设：1)交感神经活动过度是活动期溃疡性结肠炎(UC)的特征，2)可乐定降低交感神经活动与UC的临床变化有关。23例UC患者和20例对照组连续记录肌交感神经活动(MSNA)、心电图、血压和呼吸，并在安静和75度仰卧位时测定血浆儿茶酚胺。通过对R-R间期和收缩压变异性的频谱分析，通过MSNA、去甲肾上腺素、肾上腺素、低频(LF)心脏交感神经(LFRR；归一化单位)和高频(HF)副交感神经(HFRR；归一化单位)调制和交感血管运动控制(LF收缩动脉压；LFSAP)的频谱标记物来评估自主神经的变化。在UC患者中，16名患者同意随机分配给8wk的可乐定透皮吸收(15 mg/wk，9名受试者)或安慰剂(7名患者)。比较可乐定/安慰剂治疗前后的自主神经症状、疾病活动指数(DAI)和内窥镜检查结果。安静时，患者的MSNA、心率(HR)、LFRR、LF/HF、LFSAP高于对照组，HFRR低于对照组。与对照组相比，倾斜降低了HFRR，增加了MSNA和LFRR。可乐定可降低HR、MSNA、肾上腺素、LFRR，增加HFRR，而安慰剂则没有影响。可乐定治疗后自主神经功能的改变与DAI评分的降低有关。以活动期UC为特征的交感神经活动总体增强。可乐定使自主神经功能恢复正常，伴随着病情的改善。
Previous reports suggest that inflammatory bowel diseases may be accompanied by abnormalities in the neural autonomic profile. We tested the hypotheses that 1) an exaggerated sympathetic activity characterizes active ulcerative colitis (UC) and 2) a reduction of sympathetic activity by clonidine would be associated with clinical changes of UC. In 23 patients with UC and 20 controls, muscle sympathetic nerve activity (MSNA), ECG, blood pressure, and respiration were continuously recorded, and plasma catecholamine was evaluated both at rest and during a 75 degrees head-up tilt. Autonomic profile was assessed by MSNA, norepinephrine, epinephrine, spectral markers of low-frequency (LF) cardiac sympathetic (LFRR; normalized units) and high-frequency (HF) parasympathetic (HFRR; normalized units) modulation and sympathetic vasomotor control ( LF systolic arterial pressure; LFSAP), obtained by spectrum analysis of the R-R interval and systolic pressure variability. Among UC patients, 16 agreed to be randomly assigned to 8-wk transdermal clonidine ( 15 mg/wk, 9 subjects), or placebo ( 7 patients). An autonomic profile, Disease Activity Index (DAI), and endoscopic pattern were compared before and after clonidine/placebo. At rest, MSNA, heart rate (HR), LFRR, LF/HF, and LFSAP were higher and HFRR was lower in patients than in controls. Tilt decreased HFRR and increased MSNA and LFRR less in patients than in controls. Clonidine decreased HR, MSNA, epinephrine, LFRR, and increased HFRR, whereas placebo had no effects. Changes of the autonomic profile after clonidine were associated with reduction of DAI score. An overall increase of sympathetic activity characterized active UC. Normalization of the autonomic profile by clonidine was accompanied by an improvement of the disease.