Case Report
Copyright ©The Author(s) 2015.
World J Gastrointest Pathophysiol. Nov 15, 2015; 6(4): 243-248
Published online Nov 15, 2015. doi: 10.4291/wjgp.v6.i4.243
Table 2 List of observations associating electrical nerve stimulations and the development of acute pancreatitis
Ref.
Observation
All cases reported here were considered idiopathicN/A
There was a strong temporal association of exposure and APN/A
There was a directly proportional relationship between duration of exposure and severity of subsequent APN/A
Neurogenic inflammation is increasingly recognized to play a role in development of AP, with sensory nerves in particular being considered a final common pathway in AP[24,30,39,40]
TRPV1 and TRPA1 expression and function in pancreatic afferent neurons increases and blocking this pathway attenuates pancreatitis in a mouse model of AP[25,26]
Over-stimulation of nerves associated with pancreatic disease (decrease in pancreatic blood flow and DNA synthesis) in rats[34]
Neural cross talk between the duodenum and pancreas (duodeno-pancreatic reflex at T6-T13) can promote AP in a rat model[41]
Possibly contradictory observations
Stimulation by electroacupuncture of dorsal segmental points corresponding to levels that innervate pancreas (by splanchnic nerves; T9-T11) causes decrease in fasting blood glucose[33]
Electroacupuncture protects against CCK-induced AP in rats[31]
Electroacupuncture to paraumbilical point ST25 (dermatome T10) down-regulates pro-inflammatory cytokines (TNFα, IL-6) and attenuates the morphological damage to pancreas in a rat model of AP[32]