Energetic etiologies of acute pancreatitis: A report of five cases

Table 2 List of observations associating electrical nerve stimulations and the development of acute pancreatitis

	Ref.
Observation
All cases reported here were considered idiopathic	N/A
There was a strong temporal association of exposure and AP	N/A
There was a directly proportional relationship between duration of exposure and severity of subsequent AP	N/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]

AP: Acute pancreatitis; N/A: Not available; TNF: Tumor necrosis factor; IL- 6: Interleukin- 6; TRPV1: Transient receptor potential vanilloid 1; TRPA1: Transient receptor potential cation channel, subfamily A, member 1; CCK: Cholecystokinin.