VAGAL-STIMULATION INDUCES INCREASED PULMONARY VASCULAR-PERMEABILITY IN GUINEA-PIG

The effects of vagal stimulation on pulmonary vascular permeability we re studied in guinea pigs in vivo using I-125-labeled albumin as a mar ker of plasma extravasation. Bilateral vagus nerve stimulation (NS) si gnificantly increased the plasma leakage index in both parenchyma and tracheobronchial tissues. The NS-induced plasma leakage in the parench yma was unaffected by the alpha-adrenoceptor antagonist phentolamine, the muscarinic receptor antagonist atropine, the ganglionic blocker he xamethonium, or pretreatment with 6-hydroxydopamine or capsaicin, but it was significantly potentiated by the beta-adrenoceptor antagonist p ropranolol. NS-induced tracheobronchial vascular leakage was markedly inhibited by pretreatment with atropine, hexamethonium, or capsaicin, although it was unaffected by pretreatment with phentolamine, proprano lol, or 6-hydroxydopamine. By itself, N-G-nitro L-arginine methyl este r (L-NAME), an inhibitor of nitric oxide (NO) synthase, had no effect on pulmonary vascular leakage, but it significantly enhanced the NS-in duced plasma leakage to parenchyma in a dose-related and L-arginine-re versible manner. Elevation of blood pressure to a similar extent as th at induced by L-NAME by a phenylephrine infusion had no significant ef fect on the increased plasma leakage induced by NS. These results sugg est that vagal stimulation increases plasma extravasation in lung pare nchyma through the release of unidentified transmitter(s) in a process that is modulated by endogenous NO and catecholamines (via activation of beta-adrenoceptors), and that different mechanisms are involved in the vagally induced plasma extravasation in the pulmonary and tracheo bronchial vascular beds.