ABSTRACT
Pulmonary surfactant prevents alveolar collapse by reducing alveolar surface tension and aids gaseous exchange in the lung. Since inadequate production of pulmonary surfactant is a key etiological process in ARDS, surfactant may play an important role in pathogenesis of ARDS. To provide a clue for establishing pathological mechanism of post-traumatic or neurogenic ARDS, we studied the influence of the vagal innervation on pulmonary surfactant metabolism. A total of 20 S-D rats (about 230 gm wt. each) were divided into two conditions: normal control and vagotomized groups. The vagotomized rats were subdivided into 3 hours, 8 hours and 24 hours groups. To preserve the superior cervical cardiac branches, both vagus nerves were cut at the lowest part of the carotid triangle. Cannula for adequate respiration and suction was fitted into the trachea. The lung tissue were processed for H&E, Masson's trichrome, Immunohistochemistry using anti-surfactant protein A (SP-A) and .anti-prosurfactant protein C (ProSP-C). The results were as follows; 1. The lungs of the vagotomized rats showed alveolar edema, fibrosis with infiltration of inflammatory cells and hyaline membrane formation. 2. In the lungs of the vagotomized rats, SP-A and ProSP-C immunoreactivity was decreased in proportion to postoperation time. Consequently, it can be postulated that autonomic disturbances caused by vagal interruption may induce ARDS-like pulmonary damage by modulating alveolar surfactant protein metabolism and by evoking the secondary inflammatory processes.