Important casual association of carotid body and glossopharyngeal nerve and lung following experimental subarachnoid hemorrhage in rabbits. First report

被引:30
作者
Yolas, Coskun [1 ]
Kanat, Ayhan [2 ]
Aydin, Mehmet Dumlu [3 ]
Turkmenoglu, Osman Nuri [4 ]
Gundogdu, Cemal [5 ]
机构
[1] Erzurum Reg Res & Educ Hosp, Dept Neurosurg, Erzurum, Turkey
[2] Recep Tayyip Erdogan Univ, Fac Med, Dept Neurosurg, Rize, Turkey
[3] Ataturk Univ, Fac Med, Dept Neurosurg, Erzurum, Turkey
[4] Sisli Etfal Res & Educ Hosp, Dept Neurosurg, Istanbul, Turkey
[5] Ataturk Univ, Fac Med, Dept Pathol, Erzurum, Turkey
关键词
Subarachnoid hemorrhage; Glossopharyngeal nerve; Carotid body; Brain stem compression; Cardiorespiratory arrest; Degenerative injury; ANEURYSM; VASOSPASM; GANGLION; STIMULATION; DIAGNOSIS;
D O I
10.1016/j.jns.2013.10.047
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Object: The glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. The relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied. Methods: Twenty rabbits were included in this study. Five of them (n = 5) were used as control group. The remaining animals (n = 15) were exposed to experimental SAH. In the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n = 9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated. Results: The mean number of live neurons in CBs was 4206.67 +/- 148.35 and live axons of GPNs were 1211.66 +/- 14.29 in the animals of the control group. The number of degenerated neurons of CBs was 2065 +/- 110.27 and the number of degenerated axons of GPNs was 530.83 +/- 43.48 in early killed animals with SAH. The number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89 +/- 4184 and 2270.5 +/- 13438 in the living animals with SAH, respectively. Conclusions: High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung. Crown Copyright (c) 2013 Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:220 / 226
页数:7
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