Related Experiment Videos
Megaoesophagus in rats: a clinical, pathological and morphometrical study
A Baiocco1, C E Boujon, W Häfeli
1Institute of Animal Pathology, University of Berne, Switzerland.
Journal of Comparative Pathology
|April 1, 1993
Summary
A study found that megaesophagus in Long-Evans rats involves esophageal dilation and nerve cell loss. This condition, characterized by clinical signs and histological changes, is suggested to have a hereditary cause.
Area of Science:
- Veterinary Pathology
- Gastroenterology
- Animal Models
Background:
- Megaoesophagus is a condition characterized by abnormal dilation of the esophagus.
- Understanding the underlying mechanisms and potential causes of megaesophagus in animal models is crucial for comparative medicine.
Purpose of the Study:
- To investigate the clinical, radiographic, and histological features of megaesophagus in Long-Evans rats.
- To explore the potential aetiology of megaesophagus in this specific rat strain.
Main Methods:
- Clinical examination of 82 affected Long-Evans rats (aged 3-32 months).
- Radiographic imaging with barium contrast to assess esophageal structure.
- Histological examination of esophageal tissues, focusing on muscular layers and myenteric ganglia.
- Geometrical modeling to analyze esophageal shape and ganglion cell density.
Main Results:
- Affected rats exhibited clinical signs including coarse hair, neck distension, and respiratory distress.
- Radiography revealed esophageal dilation with impacted food, varying in severity.
- Histology showed inflammation and necrosis in muscular layers, reduced myenteric ganglion cells, and decreased muscle thickness.
- Geometrical analysis ruled out shape changes as the cause for reduced ganglion cell number.
Conclusions:
- Megaoesophagus in Long-Evans rats is associated with significant structural and cellular changes in the esophagus.
- The absence of infectious disease and strain specificity suggest a hereditary basis for this condition.
- This rat model provides insights into esophageal motility disorders and their genetic underpinnings.