A model for experimental vasomotor rhinitis

Clinical and experimental observations suggest that vasomotor rhinitis results primarily from a relative overactivity of the parasympathetic nervous system; however, some questions remain unanswered. Does the autonomic imbalance produce vasomotor rhinitis through local neural effects on the mucosal and submucosal structures or is there activated a more systemic response involving, for instance, the immunologic system? Our study was designed to determine whether we could consistently produce unilateral vasomotor rhinitis in dogs by thorough ipsilateral sympathectomy and to evaluate the role that the immunologic system may have in the etiology of this disorder. Histologic observations were made on the nasal mucosa of control and sympathectomized dogs. In addition, serum and nasal wash specimens were collected for albumin and immunoglobulin analysis. When compared to that of control dogs, the nasal mucosa of sympathectomized dogs initially demonstrated epithelial discontinuity, submucosal fluid, and cellular infiltrates. There was no significant difference in mean albumin or immunoglobulin values of the nasal washings from control and sympathectomized dogs. Although not statistically significant, a trend was suggested in that serum IgA and IgG a,b levels were lower in the sympathectomized dogs. Although histologic changes suggestive of vasomotor rhinitis occurred in the sympathectomized dogs, biopsy specimens of nasal mucosa taken three months after operation did not reveal the prominent mucosal changes present one month after operation. The decrease in serum IgA and IgG a,b levels in the sympathectomized dogs suggests decreased production secondary to autonomic disturbance. The entity of vasomotor rhinitis may be contrived from several factors. The local effects of autonomic imbalance combined with alterations in immunologic competence may be of particular importance.