VAGAL AND SYMPATHETIC DENERVATION IN THE DEVELOPMENT OF OLEIC ACID-INDUCED PULMONARY-EDEMA

This study investigates the effects of autonomic denervation on extrav ascular lung water, pulmonary hemodynamics, the filtration coefficient of pulmonary vasculature and oxygenation in the development of pulmon ary edema. Thirty seven dogs were divided into seven groups. No experi mental 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 c entral vein to induce pulmonary edema: group OAc (n = 6, intact innerv ation); 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 res ults showed that in the dogs with normal lungs, bilateral vagotomy per se did not cause lung injury during 3 h of observation. However, in o leic acid pulmonary edema, vagotomy significantly deteriorated pulmona ry edema by increasing pulmonary intravascular pressures; Alpha- or al pha- 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 vagosympathect omy as in the dogs with intact innervation. These results suggest the inhibition of vagal or sympathetic innervation will aggravate pulmonar y edema in the dog. (C) 1997 Elsevier Science B.V.