Send to

Choose Destination
See comment in PubMed Commons below
Histol Histopathol. 2000 Jul;15(3):983-91.

Functional morphology of the equine pelvic flexure and its role in disease. A review.

Author information

Department of Large Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg 24061, USA.


The hindgut is the major site in the horse for nutrient digestion and absorption. Most of this activity occurs in the large intestinal compartments, i.e., cecum, right and left ventral colon and left and right dorsal colon. The colonic pelvic flexure is a short and narrow loop connecting the left ventral and left dorsal colon. It is not significant directly in digestive and absorptive processes but plays an important functional role in regulating colonic aboral and retropropulsive transit of digesta through its motility pacemaker activity. The pelvic flexure also contributes to the pathophysiology of colic, the leading cause of death in horses. Its narrow lumen may contribute to colonic impaction, and malfunctions of the pacemaker may contribute to volvuli and colonic displacements. Neuronal and ganglion density of the myenteric plexus is increased at the pelvic flexure and adjacent left dorsal colon pacemaker region. Contractile activity, vasoactive intestinal peptide (VIP) and neurokinins-1 and -3 are all enhanced in the pelvic flexure. The mucosa histologically resembles that of the ventral and dorsal colon, with apically-granulated principal cells and goblet cells lining the luminal surface. Clustered intranuclear inclusions resembling the cytoplasmic granules are also observed by electron microscopy in the principal cells as elsewhere in the horse colon. Further neuroendocrine and morphologic investigation of the pelvic flexure is warranted due to the great importance of this localized region for normal function and pathophysiology.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center