7 research outputs found
A New Determinant of Poor Outcome After Spontaneous Subarachnoid Hemorrhage: Blood pH and the Disruption of Glossopharyngeal Nerve-Carotid Body Network: First Experimental Study
AYDIN, Nazan/0000-0003-3232-7713; Kanat, Ayhan/0000-0002-8189-2877WOS: 000407713100045PubMed: 28456740OBJECTIVE: 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/mm(3) and the degenerated neuron density was 11 +/- 3/mm(3), whereas the degenerated neuronal density in CBs was 35 +/- 8/mm(3) in the sham group and 1034 +/- 112/mm(3) in the slight acidosisedeveloped group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 +/- 251/mm(3) in the prominent acidosise developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 +/- 840/mm(3). 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