First report of vagal ischemia induced lung immune componenet infarct following subarachnoid hemorrhage: experimental study

Abstract

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

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

“…Vagal ischemia may be a causative role on the pathogenesis of NLE. Degenerated vagal complex may be a causative factor in the lymph node infarct in SAH 11 . Failure hilar parasympathetic ganglia may be responsible for pulmonary vasospasm in lungs.…”

Stellate ganglion ischemia on the prevention of pulmonary vasospasm during bilateral carotid artery ligation: The first experimental study

“…Vagal complex degeneration induces glomerular atrophy based on relative sympathetic overactivity . The degenerated vagal complex may be a causative factor in the development of pulmonary immune deficiency …”

A Review of the Mysterious Roles of the Autonomic Ganglia Considered as Deep Intelligence Agency in the United States of the Brain

“…Nodose ganglia are conveyed from visceral afferent signals via vagal nerves to the brainstem and higher brain centers such as the insula. The nodose ganglia, stellate ganglia, and intrinsic cardiac ganglia disturbances can lead to burned neurocardiac web syndrome, 9 neurogenic stunned myocardium, 10 acutely-developed nontreatable hyperglycemia, 11 pulmonary lymph node infarts, 12 coronary vasospasm 13 and also cardiac arrest following subarachnoid hemorrhage. 14 The low neuron density of the hilar parasympathetic ganglia of vagal nerves may be responsible for pulmonary artery vasospasm and neurogenic lung edema following subarachnoid hemorrhage.…”