Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). Because vagal nerves have vital roles in the lung functions, vagal ischemia may be a causative role on the pathogenesis of NPE. We examined whether there was a relationship between the vagal complex ischemia and lung immune complex occupying lymph node infarct in SAH.Material and Methods:
Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH applied group (n=22) by way of autologous blood injection to cisterna magna and followed three weeks. The ratio of the lung lymph node arteries (LLNA) wall sectioning (wall ring) surface to the lumen surface was considered vasospasm index (VSI). Degenerated axon numbers of vagal nerves and neuron densities of nodose ganglion (NG) and vasospasm indexes of LLNA were compared among the groups.Results:
The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm2, 30±5/mm3, and 0.777±0.048 in the control group; 1300±100/mm2, 720±90/mm3, and 1.148±0.090 in the animals with slight vasospasm (n=12); and 7300±530/mm2, 5610±810/mm3, and 1.500±0.120 in the animals with severe vasospasm (n=10), respectively.Conclusion:
Degenerated vagal axon and NG neuron density may be a causative factor in the development of LLNA vasospasm induced lymph node infarct in SAH; and, lung lymph node infarcts may be an important factor on the prognosis of NPE.