Background: Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether subarachnoid hemorrhage causes dissection, or not. This study aims to investigate the relationship between, degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery.
Material and Method: In this article, after three weeks of experimental SAH, animals were decapitated. 18 rabbits were divided into three groups, according to their vasospasm indexes. The basilar arteries were examined by anatomical and histopathological methods.
Results: Basilar dissection with high vasospasm index value (VSI>3) was detected in six animals (G-I, n=6); severe basilar edema and moderate vasospasm index value (VSI>2.4) in seven rabbits (G-II, n=7) and slight vasospasm (VSI<1.5) index value in five subjects (G-III, n=5) was detected. The degenerated neuron densities (n/mm3) of the superior cervical ganglia were detected as 12±4 in G-I, 41±8 in G-II; and 276±78 in G-III. The dissected surface values/lumen values were calculated as (42±1)/(64±11) in G-I; (21±6)/(89±17) in G-II; and (3±1)/(102±24) in G-III. If we look at these ratios as a percentage: 62%in G-I, 23% in G-II, and 5% in G-III.
Conclusion: Inverse relationship between the degenerated neuron densities (n/mm3) of the superior cervical ganglia and the dissected surface values basilar artery was observed. The common knowledge is that basilar artery dissection may lead to SAH, however, this study indicates that SAH is the cause of basilar artery dissection.
Fatal pulmonary edema and hemorrhage are significant complications of endovascular treatment in steno-occlusive carotid artery disease; a rational mechanism has not been adequately examined in the literature so far. We investigated if cervical sympathetic ganglia ischemia prevents pulmonary vasospasm on the prognosis of bilateral common carotid artery ligation (BCCAL). Twenty-three adult New Zealand rabbits (4.2 AE 0.3 kg) were randomly divided into three groups: the control group (G1, n = 5), the sham group (G2, n = 6), and the BCCAL group (G3, n = 12). Common carotid arteries were dissected bilaterally in G2/G3, and permanent BCCAL was applied to only in G3. All animals were followed for 3 weeks and decapitated under general anesthesia. Histopathological changes in stellate ganglia and severity of pulmonary vasospasm-related lung edema and hemorrhage were investigated. Results were analyzed by the Kruskal-Wallis test. Two animals of G3 dead within three weeks and the remainder were sacrificed three weeks later. Subpleural petechial foci and an endotracheal bloody fluid collection were grossly observed in the lungs. Histopathologically, pulmonary artery vasospasm, perivascular and subintimal edema, interalveolar hemorrhage, and alveolar wall destructions were observed with less ischemic-degenerated neuron density-determined stellate ganglia animals. Neurodegeneration of stellate ganglia may have a beneficial effect on the prevention of lung injury during stenoocclusive carotid artery disease.
Aim: Scalp hairs are mainly innervated by sensitive fibers of trigeminal nerves. Ischemic neurodegeneration of trigeminal ganglion can cause denervation injury of scalp hairs. We investigated if there is a relationship between the degenerated neuron densities of trigeminal ganglion neuron densities and the numbers of degenerated hair follicles numbers following subarachnoid hemorrhage (SAH).
Material and Method: Five normal (n=5), five SHAM (n=5), and ten (n=10) male rabbits were chosen from formerly experimental SAH created by cisternal homologous blood injection (0.75cc) group, which followed for three weeks. Degenerated neuron numbers of trigeminal ganglion and atrophic hair follicles numbers in the frontal areas of the scalp were examined by stereological methods. Degenerated neuron densities of trigeminal ganglions and atrophic hair follicles numbers were analyzed by the Mann-Whitney U test.
Results: The mean degenerated neuron densities trigeminal ganglions (n/mm3) and atrophic hair follicles (n/mm2) were determined as 5±2/m3 and12±4/mm2 in control; 12±3/m3 and 41±8/mm2 in Sham and, 168±23/m3 and 79±14/mm2 in the study group (p>0.001). In the post-hoc analysis, all groups differed significantly from each other. A linear association was observed between the degenerated neuron densities of trigeminal ganglions and atrophic hair follicles (r: 0.343, p: 0.007).
Conclusion: Trigeminal ganglion neurodegeneration may be an essential factor in hair follicles atrophy after SAH, which has not been mentioned in the literature so far.
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