Subglottic stenosis occurs as a complication of prolonged endotracheal intubation secondary to inflammation with development of scar tissue and subsequent fibrosis. Collagen I and III levels increase during the healing process. Steroids alter the inflammatory response, decreasing recruitment of macrophages and fibroblasts. beta-Aminopropionitrile (beta APN) inhibits the development of collagen cross-linking. A mechanism that would minimize hypertrophic set-ring was sought. Eighteen dogs were anesthetized, had tracheostomies performed, and later had cautery of the mucosa and inner layer of the cricoid cartilage. Of 18 survivors, 6 animals were used as controls, 6 animals received oral Decadron, 2 mg/d, and 6 animals received oral beta APN, 40 mg/d. There were 9 early deaths - 5 in the steroid group. Animals were painlessly sacrificed, and the specimens were sectioned at the cricoid cartilage level and were stained immunohistochemically for antibodies to collagen types I to VI. Analysis of the area of scar and the intensity of stain was performed with Mocha image analysis software. Collagen III increased in control animals to 14.35 +/- 1.85 (intensity stain index), but this reaction was reduced by beta APN (5.77 +/- 1.78, p < .01). Steroids had no significant effect on formation of any type of collagen. Lathyrogens (beta APN) may offer a pharmacologic tool to reduce scar tissue.