Abstract：
OBJECTIVE: This study aimed to investigate the integrative effects and mechanisms of transcutaneous electrical acustimulation (TEA) on postprocedural recovery from endoscopic retrograde cholangio-pancreatography (ERCP).
METHODS: A total of 86 patients for elective ERCP were randomly ordered to receive TEA (n = 43) at acupoints PC6 and ST36 or Sham-TEA (n = 43) at sham points from 24 hours before ERCP (pre-ERCP) to 24 hours after ERCP (PE24). Scores of gastrointestinal (GI) motility-related symptoms and abdominal pain, gastric slow waves, and autonomic functions were recorded through the spectral analysis of heart rate variability; meanwhile, circulatory levels of inflammation cytokines of tumor necrosis factor-α (TNF-α) and interleukin (IL)-10 and GI hormones of motilin, ghrelin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) were assessed by enzyme-linked immunosorbent assay.
RESULTS: 1) TEA, but not Sham-TEA, decreased the post-ERCP GI motility-related symptom score (2.4 ± 2.6 vs 7.9 ± 4.6, p < 0.001) and abdominal pain score (0.5 ± 0.7 vs 4.1 ± 2.7, p < 0.001) at PE24, and decreased the post-ERCP hospital day by 20.0% (p ＜0.05 vs Sham-TEA); 2) TEA improved the average gastric percentage of normal slow waves and dominant frequency by 34.6% and 33.3% at PE24, respectively (both p < 0.001 vs Sham-TEA); 3) TEA, but not Sham-TEA, reversed the ERCP-induced increase of TNF-α but not IL-10 at PE24, reflected as a significantly lower level of TNF-α in the TEA group than in the Sham-TEA group (1.6 ± 0.5 pg/mL vs 2.1 ± 0.9 pg/mL, p ＜ 0.01); 4) compared with Sham-TEA, TEA increased vagal activity by 37.5% (p ＜ 0.001); and 5) TEA caused a significantly higher plasma level of ghrelin (1.5 ± 0.8 ng/ml vs 1.1 ± 0.7 ng/ml, p ＜ 0.05) but not motilin, VIP, or CCK than did Sham-TEA at PE24.
CONCLUSIONS: TEA at PC6 and ST36 accelerates the post-ERCP recovery, reflected as the improvement in GI motility and amelioration of abdominal pain, and suppression of the inflammatory cytokine TNF-α may mediate through both autonomic and ghrelin-related mechanisms.
METHODS: A total of 86 patients for elective ERCP were randomly ordered to receive TEA (n = 43) at acupoints PC6 and ST36 or Sham-TEA (n = 43) at sham points from 24 hours before ERCP (pre-ERCP) to 24 hours after ERCP (PE24). Scores of gastrointestinal (GI) motility-related symptoms and abdominal pain, gastric slow waves, and autonomic functions were recorded through the spectral analysis of heart rate variability; meanwhile, circulatory levels of inflammation cytokines of tumor necrosis factor-α (TNF-α) and interleukin (IL)-10 and GI hormones of motilin, ghrelin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) were assessed by enzyme-linked immunosorbent assay.
RESULTS: 1) TEA, but not Sham-TEA, decreased the post-ERCP GI motility-related symptom score (2.4 ± 2.6 vs 7.9 ± 4.6, p < 0.001) and abdominal pain score (0.5 ± 0.7 vs 4.1 ± 2.7, p < 0.001) at PE24, and decreased the post-ERCP hospital day by 20.0% (p ＜0.05 vs Sham-TEA); 2) TEA improved the average gastric percentage of normal slow waves and dominant frequency by 34.6% and 33.3% at PE24, respectively (both p < 0.001 vs Sham-TEA); 3) TEA, but not Sham-TEA, reversed the ERCP-induced increase of TNF-α but not IL-10 at PE24, reflected as a significantly lower level of TNF-α in the TEA group than in the Sham-TEA group (1.6 ± 0.5 pg/mL vs 2.1 ± 0.9 pg/mL, p ＜ 0.01); 4) compared with Sham-TEA, TEA increased vagal activity by 37.5% (p ＜ 0.001); and 5) TEA caused a significantly higher plasma level of ghrelin (1.5 ± 0.8 ng/ml vs 1.1 ± 0.7 ng/ml, p ＜ 0.05) but not motilin, VIP, or CCK than did Sham-TEA at PE24.
CONCLUSIONS: TEA at PC6 and ST36 accelerates the post-ERCP recovery, reflected as the improvement in GI motility and amelioration of abdominal pain, and suppression of the inflammatory cytokine TNF-α may mediate through both autonomic and ghrelin-related mechanisms.
摘要：
目的：本研究旨在探讨经皮电刺激(TEA)对内镜逆行胰胆管造影术(ERCP)术后恢复的综合作用和机制。
方法：共有86例择期ERCP患者被随机命令在ERCP前24小时（ERCP前）至ERCP后24小时（PE24）接受PC6和ST36穴位TEA（n=43）或Sham-TEA（n=43）。胃肠道（GI）运动相关症状和腹痛的分数，胃慢波,通过心率变异性的频谱分析记录自主神经功能；同时，肿瘤坏死因子-α（TNF-α）和白细胞介素（IL）-10的炎症细胞因子和胃动素的GI激素的循环水平，ghrelin,胆囊收缩素(CCK),通过酶联免疫吸附试验评估血管活性肠肽（VIP）。
结果：1）TEA，但不是假茶,PE24时ERCP后胃肠动力相关症状评分（2.4±2.6vs7.9±4.6，p<0.001）和腹痛评分（0.5±0.7vs4.1±2.7，p<0.001），ERCP后住院天数减少20.0%（p＜0.05vsSham-TEA）；2）TEA在PE24时，正常慢波和主导频率的平均胃百分比分别提高了34.6%和33.3%（ShEA<3）但不是假茶,在PE24处逆转了ERCP诱导的TNF-α而不是IL-10的增加，反映为TEA组的TNF-α水平明显低于Sham-TEA组（1.6±0.5pg/mLvs2.1±0.9pg/mL，p＜0.01)；4)与假TEA相比，TEA使迷走神经活动增加37.5%(p＜0.001);5)TEA引起血浆ghrelin水平显著升高(1.5±0.8ng/mlvs1.1±0.7ng/ml,p＜0.05)，但不是胃动素，VIP,或CCK比PE24的Sham-TEA。
结论：TEA在PC6和ST36加速ERCP后的恢复，表现为胃肠动力的改善和腹痛的改善，炎性细胞因子TNF-α的抑制可能通过自主神经和生长素释放肽相关机制介导。
方法：共有86例择期ERCP患者被随机命令在ERCP前24小时（ERCP前）至ERCP后24小时（PE24）接受PC6和ST36穴位TEA（n=43）或Sham-TEA（n=43）。胃肠道（GI）运动相关症状和腹痛的分数，胃慢波,通过心率变异性的频谱分析记录自主神经功能；同时，肿瘤坏死因子-α（TNF-α）和白细胞介素（IL）-10的炎症细胞因子和胃动素的GI激素的循环水平，ghrelin,胆囊收缩素(CCK),通过酶联免疫吸附试验评估血管活性肠肽（VIP）。
结果：1）TEA，但不是假茶,PE24时ERCP后胃肠动力相关症状评分（2.4±2.6vs7.9±4.6，p<0.001）和腹痛评分（0.5±0.7vs4.1±2.7，p<0.001），ERCP后住院天数减少20.0%（p＜0.05vsSham-TEA）；2）TEA在PE24时，正常慢波和主导频率的平均胃百分比分别提高了34.6%和33.3%（ShEA<3）但不是假茶,在PE24处逆转了ERCP诱导的TNF-α而不是IL-10的增加，反映为TEA组的TNF-α水平明显低于Sham-TEA组（1.6±0.5pg/mLvs2.1±0.9pg/mL，p＜0.01)；4)与假TEA相比，TEA使迷走神经活动增加37.5%(p＜0.001);5)TEA引起血浆ghrelin水平显著升高(1.5±0.8ng/mlvs1.1±0.7ng/ml,p＜0.05)，但不是胃动素，VIP,或CCK比PE24的Sham-TEA。
结论：TEA在PC6和ST36加速ERCP后的恢复，表现为胃肠动力的改善和腹痛的改善，炎性细胞因子TNF-α的抑制可能通过自主神经和生长素释放肽相关机制介导。
