Kanat Ayhan, Aydin M Dumlu, Bayram Ednan, Kazdal Hizir, Aydin Nazan, Omeroglu Muhammet, Altinkaynak Konca, Kabalar M Esref, Yolas Coskun, Ozturk Cengiz, Kepoglu Umit, Calik Muhammet
Department of Neurosurgery, Recep Tayyip Erdogan University, Rize, Turkey.
Department of Neurosurgery, Medical Faculty, Ataturk University, Erzurum, Turkey.
World Neurosurg. 2017 Aug;104:330-338. doi: 10.1016/j.wneu.2017.04.105. Epub 2017 Apr 26.
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.
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 cm serum saline and 1 cm 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.
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 and the degenerated neuron density was 11 ± 3/mm, whereas the degenerated neuronal density in CBs was 35 ± 8/mm in the sham group and 1034 ± 112/mm in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm 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/mm.
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.
由舌咽神经和颈动脉体(GPN-CB)组成的化学感受器网络对血液pH值的调节至关重要。蛛网膜下腔出血(SAH)后其缺血性损伤可能导致酸中毒,但尚未得到研究。
使用23只杂种兔。将它们分为3组:5只为对照组,5只为假手术组,其余13只为研究组。假手术组和研究组分别向小脑延髓池注射1厘米血清盐水和1厘米自体动脉血。记录所有动物的血液pH值。2周后,对动物实施安乐死。通过体视学方法计数颈动脉体(CBs)正常和退化神经元的数量并进行统计学分析。
13只兔子中有2只在第二周内死亡。对照组(n = 5)的平均血液pH值为7.35±0.07,假手术组(n = 5)为7.3 /span>3±0.06,轻度酸中毒兔子(n = 6)为7.29±0.05,重度酸中毒兔子(n = 7)为7.23±0.02。对照组中,CBs的平均正常神经元密度为6432±790/mm,退化神经元密度为11±3/mm,而假手术组CBs中的退化神经元密度为35±8/mm,轻度酸中毒组(n = 6;P < 0.05)为1034±112/mm。相反,重度酸中毒动物(n = 7;P < 0.005)CBs的退化神经元密度为2134±251/mm。有趣的是,在死亡的兔子中,CB的退化神经元密度为3160±840/mm。
发现SAH后GPN-CB网络破坏继发的CB神经变性与pH值之间存在负相关,这可能导致酸中毒的发生。