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Abnormal gastrocolic response in patients with intestinal pseudo-obstruction
Archives of Internal Medicine
|March 1, 1980
Summary
Patients with chronic idiopathic intestinal pseudo-obstruction lack a normal gastrocolic response to eating. Their colonic motility does not increase after meals, indicating a neurohumoral control disorder.
Area of Science:
- Gastroenterology
- Neurogastroenterology
- Digestive Physiology
Background:
- Chronic idiopathic intestinal pseudo-obstruction (CIIP) is characterized by gastrointestinal motility disturbances.
- Previous studies demonstrated motility issues in the esophagus and small intestine of CIIP patients.
- The gastrocolic response to endogenous stimuli in CIIP remains poorly understood.
Purpose of the Study:
- To investigate the gastrocolic response to a meal in patients with chronic idiopathic intestinal pseudo-obstruction.
- To compare colonic motility in CIIP patients and normal subjects after a standardized meal.
- To assess the role of neurohumoral control mechanisms in the absence of the gastrocolic response in CIIP.
Main Methods:
- A 1,000-calorie meal was administered to normal subjects and patients with CIIP.
- Colonic motility, including spike and contractile activity, was measured.
- Response to neostigmine methylsulfate was assessed to evaluate smooth muscle responsiveness.
Main Results:
- A 1,000-calorie meal significantly increased colonic spike and contractile activity in normal subjects.
- No significant increase in colonic spike or contractile activity was observed in CIIP patients post-meal.
- CIIP patients' colonic motility responded normally to neostigmine methylsulfate, indicating cholinergic responsiveness.
Conclusions:
- The normal gastrocolic response to eating is absent in patients with chronic idiopathic intestinal pseudo-obstruction.
- This loss of response suggests a disorder in the neurohumoral control mechanisms governing gastrocolic reflexes in CIIP.
- Smooth muscle cholinergic responsiveness is preserved, implicating central or enteric neural pathways in the defect.