Intestinal Bypass and Total Parenteral Nutrition: Changes in Gut Function and Morphology

Abstract: Abolition of enteral nutrition is sometimes required in severe illness. The primary aim of the present work has been to elucidate possible changes in intestinal morphology and motor function in absence of enteral nutrition. Total absence of enteral nutrition in an isolated intestinal segment was created by bypassing the distal ileum in a rat model. Intestinal bypass causes marked circumferential atrophy, a decrease in VIP, PACAP and NPY-containing nerve cells while NOS-containing nerve cells increase in number. Furthermore, loss of enteric neurons occurs. In vitro, longitudinal smooth muscle motor response changes from cholinergic contraction and nitrergic relaxation to a non-cholinergic and non-nitrergic motor response. One-week bypassed intestine becomes temporarily supersensitive to the relaxationinducing transmitters VIP, PACAP-27 and NO. The relaxatory response returns to normal after four weeks bypass. The selectivity of the receptors, by which PACAP and VIP mediate relaxation, change after bypass. In another model for intestinal adaptation, rats were set on total parenteral nutrition (TPN). TPN results in circumferential atrophy in the jejunum, ileum and colon. Morphological atrophic changes are more pronounced in the jejunum. With the exception of a decrease in the number of submucous neurons expressing NPY-mRNA, the rest of the neuronal subpopulations studied remain unaffected. Longitudinal smooth muscle response remains unaltered to electrical field stimulation and addition of VIP, PACAP or NO-donor. Jejunal goblet cells decrease in number and ileal Paneth cells increase in size. Eosinophils increase in number in the stomach, most evident in the mucosa and submucosa. In the colon, eosinophils take a more basal position within the mucosa, interpreted as eosinophils taking a ?passive position? in response to the lack of enteral stimuli. In conclusion: Absence of enteral stimuli causes a wide range of intestinal atrophic and functional changes.