Dysfunction of pancreatic exocrine secretion after experimental spinal cord injury.

Abstract

Pancreatic exocrine dysfunction is an underdiagnosed comorbidity in individuals living with spinal cord injury (SCI) who often present cholestasis, acute pancreatitis or high levels of serum pancreatic enzymes. Parasympathetic control of pancreatic exocrine secretion (PES) is mediated in the medullary dorsal vagal complex in part through cholecystokinin (CCK) release. Our previous reports indicate high thoracic (T3-) SCI reduces vagal afferent sensitivity to GI regulatory peptides, like CCK and thyrotropin releasing hormone (TRH). To date, the effects of experimental SCI on PES are unknown. Here we investigated the modulation of PES following T3-SCI in rats. We measured PES volume and amylase concentration in control and T3-SCI rats (3-days or 3-weeks after injury) following: (i) intra-duodenal administration of a mixed-nutrient liquid meal (Ensure® ™) or (ii) central TRH injection (100 pmol) in the dorsal motor nucleus of the vagus. In a separate cohort of overnight-fasted rats, basal serum amylase levels were measured. The baseline volume of PES secretion was lower in 3-week rats destined to receive Ensure® or TRH following T3-SCI surgery compared to control. PES protein concentration was significantly reduced at baseline in 3-week T3-SCI and elevated in 3-day and 3-week T3-SCI rats postprandially but only elevated in 3-day rats following TRH microinjection. Serum amylase activity levels were elevated in 3-day T3-SCI rats and remained at similar levels post 3-weeks T3-SCI. Our data suggest that vagally-mediated regulation of multiple visceral organs is disrupted in the days and weeks following experimental SCI.