Integrative effects of transcutaneous electrical acustimulation on abdominal pain, gastrointestinal motility, and inflammation in patients with early‐stage acute pancreatitis

Abstract

Background/Aims Gastrointestinal (GI) dysmotility in acute pancreatitis (AP) aggravates inflammation and results in severe complications. This study aimed to explore effects and possible mechanisms of transcutaneous electrical acustimulation (TEA) on abdominal pain, GI dysmotility, and inflammation in AP patients. Methods Forty‐two AP patients were blindly randomized to receive TEA (n = 21) at acupoints PC6 and ST36 or Sham‐TEA (n = 21) at sham points for 2 days. Symptom scores, gastric slow waves, autonomic functions (assessed by spectral analysis of heart rate variability), circulatory levels of motilin, ghrelin, and TNF‐α were measured before and after the treatment. Sixteen healthy controls (HCs) were also included without treatment for the assessment of gastric slow waves and biochemistry. Key Results Compared with Sham‐TEA, TEA decreased abdominal pain score (2.57 ± 1.78 vs. 1.33 ± 1.02, p < 0.05), bloating score (5.19 ± 1.21 vs. 0.76 ± 0.99, p < 0.001), the first defecation time (65.79 ± 19.51 h vs. 51.38 ± 17.19 h, p < 0.05); TEA, but not Sham‐TEA, improved the percentage of normal gastric slow waves by 41.6% (p < 0.05), reduced AP severity score (5.52 ± 2.04 vs. 3.90 ± 1.90, p < 0.05) and serum TNF‐α (7.59 ± 4.80 pg/ml vs. 4.68 ± 1.85 pg/ml, p < 0.05), and upregulated plasma ghrelin (0.85 ± 0.96 ng/ml vs. 2.00 ± 1.71 ng/ml, p = 0.001) but not motilin (33.08 ± 22.65 pg/ml vs. 24.12 ± 13.95 pg/ml, p > 0.05); TEA decreased sympathetic activity by 15.0% and increased vagal activity by 18.3% (both p < 0.05). Conclusions & Inferences TEA at PC6 and ST36 administrated at early stage of AP reduces abdominal pain, improves GI motility, and inhibits inflammatory cytokine, TNF‐α, probably mediated via the autonomic and ghrelin mechanisms.

The impact of transcutaneous electrical acustimulation (TEA) on rectal distension‐induced pain in patients with irritable bowel syndrome (IBS)—A study to determine the optimal TEA delivery modalities and effects on rectal sensation and autonomic function

“…For example, a recent study found that, compared to sham-TEA, TEA at acupoints ST-36 and PC-6 improved abdominal pain (in addition to gastric motility and autonomic function) when applied in patients with early-stage acute pancreatitis. 37 In another study, TEA improved abdominal pain by 50% when applied in postoperative setting in patients recovering from surgery for gastrointestinal cancers. 38 The current study adds to this body of literature, specific to TEA, and provides refinement on the optimal TEA application methodology.…”

“…Furthermore, TEA was found effective in other conditions characterized by abdominal pain. For example, a recent study found that, compared to sham‐TEA, TEA at acupoints ST‐36 and PC‐6 improved abdominal pain (in addition to gastric motility and autonomic function) when applied in patients with early‐stage acute pancreatitis 37 . In another study, TEA improved abdominal pain by 50% when applied in postoperative setting in patients recovering from surgery for gastrointestinal cancers 38 .…”

Efficacy and safety of neostigmine on treating gastrointestinal dysmotility in severe acute pancreatitis patients: study protocol for a randomized controlled trial

“…Spontaneous defection is usually an indicator for starting EN in clinical practice and is widely used in researches on gastrointestinal obstruction [31][32][33]. One [34] research investigating transcutaneous electrical acustimulation for treating acute pancreatitis used first defection time as an important endpoint. In this study, we choose the first defection time as our primary outcome.…”

Multi-targeting regulation of auricular vagus nerve stimulation on gastric hypersensitivity and gastric dysmotility in a rodent model of functional dyspepsia

“…Injury or inflammation can lead to persistent peripheral input and sensitization. [24] The lowgrade inflammatory is considered as the important pathogenesis of FD. That acute infections, food antigens, acid, and capsaicin can alter the steady state of the gastrointestinal tract and lead to dysfunction of the intestinal epithelial barrier, increasing mucosal permeability.…”

“…[25][26][27] Proinflammatory cytokines, chemokines, biogenic amines, bradykinins, prostaglandins, SP and several neurosurgeons are among the facilitatory mediators of the inflammation. [24] It has been demonstrated that SP and its neurokinin-1 receptor play a significant role in nociceptive perception that contributes to visceral hypersensitivity. [28] Yin et al found that visceral pain from irritable bowel syndrome can be relieved via mechanisms involving downregulation of SP in rats.…”