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- Ayhan Kanat, M Dumlu Aydin, Ednan Bayram, Hizir Kazdal, Nazan Aydin, Muhammet Omeroglu, Konca Altinkaynak, M Esref Kabalar, Coskun Yolas, Cengiz Ozturk, Umit Kepoglu, and Muhammet Calik.
- Department of Neurosurgery, Recep Tayyip Erdogan University, Rize, Turkey. Electronic address: ayhankanat@yahoo.com.
- World Neurosurg. 2017 Aug 1; 104: 330-338.
ObjectiveThe 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.MethodsTwenty-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.ResultsTwo 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.ConclusionAn 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.Copyright © 2017 Elsevier Inc. All rights reserved.
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