ABSTRACTof the vagal nerves (34), glossopharyngeal nerves (GPN), and cervicothoracic spinal ganglia (32).The respiratory and immunoregulatory roles of vagal nerve on the lungs (18) may be damaged (37) due to vagal nerve injury in subarachnoid hemorrhage SAH (6) and pulmonolymphatic vessel innervation deficiency resulting in lung immune defects (31). Hypoxia induces pulmonary vasoconstriction (32) and immune deficiency in the lungs (8). At the beginning of SAH, ischemic neurons of the vagal nerves generate uncontrollable parasympathetic discharges leading to lung edema associated with dilated lung lymph node arteries (LLNA) and increased vagal cholinergic activity, and consequently to cardiorespiratory hypertension (5,10). Neurogenic pulmo-█ INTRODUCTION T he lymph nodes are the most important integral part of the lung's immune system when coping with foreign bodies, metabolites and dangerous compounds. The pulmonary lymphatic system is involved in immune homeostasis and surveillance (14). Cholinergic pathways are localized in the lung lymphoid tissues, which play an important role in the modulation of neuronal metabolism and immunity in the lungs (9). The lungs are innervated by vagal, cervical sympathetic, and thoracic somatic nerves that are primarily responsible for the continuation of respiration reflexes (11). Sensory innervation of the respiratory tract is regulated primarily at the level of the nodose ganglion (NG) and pulmonary microganglia AIm: Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of NPE. We examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct in SAH. mATERIAl and mEThODS: Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH group (n=22). SAH was created by autologous blood injection into the cisterna magna and followed-up for 3 weeks. Vasospasm index (VSI) was defined as the ratio of the lung lymph node arteries (LLNA) wall section (wall ring) surface to the lumen surface. Degenerated axon numbers of vagal nerves, neuron densities of the nodose ganglion (NG) and VSIs of LLNA were compared for all groups.
RESUlTS:The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm 2