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

Abstract 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...

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Veröffentlicht in:Journal of the neurological sciences 2014-01, Vol.336 (1), p.220-226
Hauptverfasser: Yolas, Coskun, Kanat, Ayhan, Aydin, Mehmet Dumlu, Turkmenoglu, Osman Nuri, Gundogdu, Cemal
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Sprache:eng
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Zusammenfassung:Abstract 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 ± 134.38 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.
ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2013.10.047