Gastroduodenal motility

The neuromuscular function of the stomach and duodenum provides the mechanical forces that drive digestion and are responsible for sensations of satiety and of dyspepsia. This article reviews (1) the neuroendocrine factors controlling upper gastrointestinal motility, (2) noninvasive techniques to evaluate gastroduodenal motility, and (3) the pathophysiology and treatment of gastroparesis.

Nutrients in the duodenum inhibit gastric emptying via a feedback pathway that involves release of cholecystokinin and serotonin (5-HT) from neuroendocrine cells; both act peripherally, cholecystokinin via cholecystokinin A receptors and serotonin via 5-HT3 receptors. The dorsal vagal complex plays a central role in the gastric inhibition mediated by tumor necrosis factor-alpha. The construction of maps that define intestinal movements in time and space has now been extended to the stomach. MRI compares favorably with the barostat in assessing gastric volume accommodation to meals and drugs and has the advantage of being noninvasive and showing contractions. Gastroparesis is increasingly recognized as a complication of end-stage liver disease; ascites plays no role in this, but portal hypertension stiffens the gastric walls and creates hypoxic conditions that may interfere with the neuromuscular functions of the stomach. Promising for the treatment of gastroparesis are clonidine, sildenafil, and intrapyloric botulinum toxin. Electrical stimulation triggers a vagally mediated relaxation of the stomach.

Drugs may be designed that specifically act on 5-HT3, cholecystokinin, or TNF-alpha receptors. Spatiotemporal maps should boost the diagnostic yield from dynamic imaging of motility using ultrasound, computed axial tomography scan, or MRI and the understanding of the mechanical forces driving digestion. Symptomatic benefit in gastroparesis may derive more from improved accommodation than gastric emptying.