Ayhan Kanat1, M Dumlu Aydin2, Ednan Bayram3, Hizir Kazdal4, Nazan Aydin5, Muhammet Omeroglu6, Konca Altinkaynak7, M Esref Kabalar8, Coskun Yolas9, Cengiz Ozturk10, Umit Kepoglu11, Muhammet Calik12. 1. Department of Neurosurgery, Recep Tayyip Erdogan University, Rize, Turkey. Electronic address: ayhankanat@yahoo.com. 2. Department of Neurosurgery, Medical Faculty, Ataturk University, Erzurum, Turkey. 3. Department of Cardiology, Medical Faculty, Ataturk University, Erzurum, Turkey. 4. Department of Anesthesiology and Reanimation, Medical Faculty, Recep Tayyip Erdogan University, Rize, Turkey. 5. Department of Psychiatry, Bakirkoy Mental Diseases Education Hospital, Istanbul, Turkey. 6. Clinic of Neurosurgery, Agri State Hospital, Agri, Turkey. 7. Department of Biochemistry, Erzurum Research Training Hospital, Erzurum, Turkey. 8. Department of Pathology, Erzurum Research Training Hospital, Erzurum, Turkey. 9. Department of Neurosurgery, Erzurum Research Training Hospital, Erzurum, Turkey. 10. Osmangazi Family Health Center, Osmangazi Family Medicine Center, Erzurum, Turkey. 11. Department of Neurosurgery, Medical Faculty, Bahcesehir University, Istanbul, Turkey. 12. Department of Pathology, Medical Faculty, Ataturk University, Erzurum, Turkey.
Abstract
OBJECTIVE: The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insults after subarachnoid hemorrhage (SAH), which may contribute to acidosis, have not been investigated. METHODS: Twenty-three hybrid rabbits were used. They were divided into 3 groups: 5 as a control group, 5 as a sham group, and the remaining 13 as the study group. Injections included 1 cm3 serum saline and 1 cm3 autolog arterial blood into the cisterna magna in the sham and study group, respectively. Blood pH values of all animals were recorded. After 2 weeks, animals were euthanized. The number of normal and degenerated neurons of the carotid bodies (CBs) was counted by stereologic methods and analyzed statistically. RESULTS: Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35 ± 0.07 in the control group (n = 5), 7.33 ± 0.06 in the sham group (n = 5), 7.29 ± 0.05 in rabbits with slight acidosis (n = 6), and 7.23 ± 0.02 in rabbits with prominent acidosis (n = 7). In the control group, the average normal neuronal density of the CBs was 6432 ± 790/mm3 and the degenerated neuron density was 11 ± 3/mm3, whereas the degenerated neuronal density in CBs was 35 ± 8/mm3 in the sham group and 1034 ± 112/mm3 in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm3 in the prominent acidosis-developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 ± 840/mm3. CONCLUSION: An inverse relationship between neurodegeneration in the CB and pH values secondary to the disruption of the GPN-CB network after SAH was found, which may contribute to developing acidosis.
OBJECTIVE: The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insults after subarachnoid hemorrhage (SAH), which may contribute to acidosis, have not been investigated. METHODS: Twenty-three hybrid rabbits were used. They were divided into 3 groups: 5 as a control group, 5 as a sham group, and the remaining 13 as the study group. Injections included 1 cm3 serum saline and 1 cm3 autolog arterial blood into the cisterna magna in the sham and study group, respectively. Blood pH values of all animals were recorded. After 2 weeks, animals were euthanized. The number of normal and degenerated neurons of the carotid bodies (CBs) was counted by stereologic methods and analyzed statistically. RESULTS: Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35 ± 0.07 in the control group (n = 5), 7.33 ± 0.06 in the sham group (n = 5), 7.29 ± 0.05 in rabbits with slight acidosis (n = 6), and 7.23 ± 0.02 in rabbits with prominent acidosis (n = 7). In the control group, the average normal neuronal density of the CBs was 6432 ± 790/mm3 and the degenerated neuron density was 11 ± 3/mm3, whereas the degenerated neuronal density in CBs was 35 ± 8/mm3 in the sham group and 1034 ± 112/mm3 in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm3 in the prominent acidosis-developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 ± 840/mm3. CONCLUSION: An inverse relationship between neurodegeneration in the CB and pH values secondary to the disruption of the GPN-CB network after SAH was found, which may contribute to developing acidosis.
Authors: Hatice B Polat; Ayhan Kanat; Fatma B Celiker; Ahmet Tufekci; Mehmet Beyazal; Gizem Ardic; Arzu Turan Journal: Ann Indian Acad Neurol Date: 2020 Jan-Feb Impact factor: 1.383