Esophageal Achalasia Induced in Dogs by Prolonged Acrylamide Administration

Tatsuro Nakagawa, Yasuto Fujisaki, Kenji Sakurai

The First Department of Surgery, The Jikei University School of Medicine

Twenty dogs orally given acrylamide developed an esophageal achalasia-like lesion, and esophageal motility and axonal degeneration of the vagus nerve were investigated electrophysiologically and electron microscopically. From 7 weeks after the start of acrylamide administration, vomiting, diarrhea and weight loss were observed in addition to neurological distrubances such as ataxia and muscle weakness of the hind limbs. The largest transverse diameter of the lower esophagus was 16.8±1.85 mm in the control group and was significantly (p<0.01) increased to 28.9±2.26 mm in the late stage of administration in the treated group. Lower esophageal sphincter pressure (LESP) was significantly (p<0.01) increased to 29.6±4.4 cmH₂O in the treated goup. By a set of electrodes stimulating the cervical vagus nerve, the percentage of the fall values [(LESP-LESP with vagal stimulation)/LESP)×100%] was decreased significantly in the treated group. The coefficient of variation of the R-R interval in ECGs was 1.49±1.09% in the control group and was significantly (p<0.05) decreased to 0.77±0.45% in the treated group. In the histologic examination, no changes in the esophageal ganglionic cells were observed in the treated group. Axonal degeneration of the vagus nerve in the treated group was revealed by electron microscopy. From these observations it seems mandatory to seek the cause of esophageal achalasia not only in the esophageal ganglionic cells but also in the central to peripheral nervous system.

Key words
lower esophageal sphincter pressure, esophageal achalasia, manometry, acrylamide, axonopathy

Reprint requests
Tatsuro Nakagawa The First Department of Surgery, The Jikei University School of Medicine
3-25-8 Nishi-Shinbashi, Minato-ku, Tokyo, 105 JAPAN

Accepted
March 11, 1992

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