Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: an Experimental Study

Abstract Background Autonomous innervations of the lungs are maintained by cervical sympathetics and vagal nerves. Sympathetic overactivity induced neurogenic pulmonary edema(NPE) isknown as a serious complication of subarachnoid hemorrhage(SAH), but the rational neuronal mechanism of that overactivity has not yet been fully clarified. The aim of this study was to examine whether there is a relationship between vagal nerve ischemia related sympathetic overactivity and neurogenic pulmonary edema in subarachnoid hemorrhage. Methods This study was conducted on 27 rabbits. A control group was formed of 5 animals, a SHAM group of 7 to which saline was administered, and a study group of 15 animals which were injected with homologous blood into the cisterna magna. Electrocardiography and respiratory rhythm parameters were monitored for 3 weeks and the animals were then decapitated. Statistical analysis was made of the numbers of degenerated axons in the pulmonary branches of the vagal nerves, the neuron density of stellate ganglions and the vasospasm index(VSI) of the pulmonary arteries. Results In the control group, the normal respiration rate was 34±6 bpm, total axon number was 1600±270/mm2 , degenerated axon number was 10±3/mm2 , and VSI was 1.34±0.25. The SHAM group values were 30±3 bpm, 163±47/mm2 and 1.95±0.45 and the study group values were determind as 45±8 bpm, 530±92/mm2 and 2.76±0.83. The mean stellate ganglion neuron density was evaluated as 8.112±1.230/mm3 in all animals, as 7.420±410/mm3 in slight NPE and as 12.512±1236/mm3 in severe NPE developed animals. Conclusion High neuron density of stellate ganglion may have important roots in sympathetic overactivity related NPE development in SAH.