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

BACKGROUND

Autonomous innervations of the lungs are maintained by cervical sympathetic and vagal nerves. Sympathetic overactivity-induced neurogenic pulmonary edema (NPE) is known as a serious complication of subarachnoid hemorrhage, but the rational neuronal mechanism of that overactivity has not yet been clarified fully. 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 that were injected with homologous arterial 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 of the pulmonary arteries.

RESULTS

In the control group, the normal respiration rate was 34 ± 6 bpm, total axon number was 1600 ± 270/mm(2), degenerated axon number was 10 ± 3/mm(2), and vasospasm index was 1.34 ± 0.25. The sham group values were 30 ± 3 bpm, 163 ± 47/mm(2), and 1.95 ± 0.45 and the study group values were 45 ± 8 bpm, 530 ± 92/mm(2), and 2.76 ± 0.83. The mean stellate ganglion neuron density was evaluated as 8.112 ± 1.230/mm(3) in all animals, as 7.420 ± 4.10/mm(3) in animals with slight NPE, and as 12.512 ± 1.236/mm(3) in animals that developed severe NPE.

CONCLUSION

High neuron density of stellate ganglion may have important roots in sympathetic overactivity-related NPE development in subarachnoid hemorrhage.