Title of article :
A reduction in interstitial cells of Cajal in horses with equine dysautonomia (grass sickness)
Author/Authors :
Neil Hudson، نويسنده , , Ian Mayhew، نويسنده , , Geoffrey Pearson، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2001
Pages :
8
From page :
37
To page :
44
Abstract :
Equine dysautonomia (grass sickness) is a common, frequently fatal disease of horses characterised by dysfunction of the gastrointestinal tract. Interstitial cells of Cajal are the c-Kit-immunoreactive cells responsible for the generation of pacemaker activity in gastrointestinal smooth muscle. Impairment of this pacemaker action has been implicated in several motility disorders in humans and laboratory mammals. The aim of this study was to test the hypothesis that changes in interstitial cells of Cajal may be involved in the pathophysiology of the intestinal dysfunction observed in equine grass sickness. Interstitial cells of Cajal were identified using immunohistochemical labelling with an anti-c-Kit antibody and their density was assessed using a semi-quantitative grading system. Segments of ileum were examined from 24 horses free from gastrointestinal disease and compared to tissues from 28 horses with grass sickness. Segments of the pelvic flexure region of the large colon were examined from 13 horses free from gastrointestinal disease and compared to tissues from 10 horses with grass sickness. In horses with grass sickness, interstitial cells of Cajal were significantly decreased in both the myenteric plexus and circular muscle regions of both ileum and pelvic flexure compared to normal animals. Therefore, it is possible that the decline in interstitial cells of Cajal may be an important factor in the development of intestinal dysmotility observed in grass sickness.
Keywords :
colon , ileum , interstitial cells of Cajal , Equine dysautonomia
Journal title :
Autonomic Neuroscience: Basic and Clinical
Serial Year :
2001
Journal title :
Autonomic Neuroscience: Basic and Clinical
Record number :
475430
Link To Document :
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