Vagal and sympathetic denervation in the development of oleic acid-induced pulmonary edema.

This study investigates the effects of autonomic denervation on extravascular lung water, pulmonary hemodynamics, the filtration coefficient of pulmonary vasculature and oxygenation in the development of pulmonary edema. Thirty seven dogs were divided into seven groups. No experimental treatment was conducted in group Nc (n = 4, sham operation) or group Nv (n = 6, bilateral vagotomy) during a 3 h observation period. In the following groups, oleic acid (0.06 ml/kg) was injected into a central vein to induce pulmonary edema: group OAc (n = 6, intact innervation); group OAv (n = 6, bilateral vagotomy); group OAa (n = 6, alpha-blockade by phentolamine); group OAs (n = 6, alpha- and beta-blockade by sympathectomy); and group OAvs (n = 3, vagosympathectomy). The results showed that in the dogs with normal lungs, bilateral vagotomy per se did not cause lung injury during 3 h of observation. However, in oleic acid pulmonary edema, vagotomy significantly deteriorated pulmonary edema by increasing pulmonary intravascular pressures; Alpha- or alpha- and beta- sympathetic inhibition deteriorated pulmonary edema by increasing pulmonary microvascular permeability. The severity of oleic acid-induced pulmonary edema was same in the dogs with vagosympathectomy as in the dogs with intact innervation. These results suggest the inhibition of vagal or sympathetic innervation will aggravate pulmonary edema in the dog.