title: The contribution of chemoreceptor-network injury to the development of respiratory arrest following subarachnoid hemorrhage.
abstract: OBJECTIVE
  Respiratory arrest following brainstem herniation has been attributed to injuries resulting from compression of the respiratory centers. While it is widely perceived that the chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the modulation of respiration, its contribution to the development of respiratory arrest has not been investigated. Therefore, the aim of this study was to investigate whether injury to the GPN-CB occurs in animals with respiratory arrest caused by experimentally-induced subarachnoid hemorrhage.
  
  
  METHODS
  Eighteen hybrid rabbits were used in this study. Four rabbits (n=4) were used to determine the normal structure of the GPN-CB. The remaining rabbits (n=14) received an autologous blood injection into the cisterna magna to produce a subarachnoid hemorrhage, after which they were observed for 20 days. The number of axons and the neuron density in the glossopharyngeal nerve and carotid body, respectively, were counted by stereological methods. The Mann-Whitney U test was used to analyze the results.
  
  
  RESULTS
  Six of 14 rabbits died within the first week, likely due to brain swelling and crushing injuries that were observed in the brain stem and related structures. In control rabbits, the average neuronal density of the carotid body was 4250 ±1250/mm(3), while the axonal density in the glossopharyngeal nerve was 18000±5100 mm(2). Conversely, in the dead rabbits, the degenerated neuron density of the carotid body was 2100±500/mm(3), while the degenerated axon density in the glossopharyngeal nerve was 8500±2550 mm(2). In addition, histopathological lesions were more severe in the dead rabbits in terms of their glossopharyngeal nerve and carotid body.
  
  
  CONCLUSIONS
  There is an important relationship between neurodegeneration in the GPN-CB and mortality rates following experimentally-induced hemorrhage. This relationship suggests that injury to the GPN-CB network disrupts the breathing reflex and results in respiratory arrest following a subarachnoid hemorrhage (SAH).
authors.affiliation: Department of Neurosurgery, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Mehmet Dumlu
authors.initials: MD
authors.lastname: Aydin
authors.affiliation: Thoracic Surgery, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Atilla
authors.initials: A
authors.lastname: Eroglu
authors.affiliation: Thoracic Surgery, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Atila
authors.initials: A
authors.lastname: Turkyilmaz
authors.affiliation: Anesthesiology and Reanimation, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Ali Fuat
authors.initials: AF
authors.lastname: Erdem
authors.affiliation: Anesthesiology and Reanimation, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Hacı Ahmet
authors.initials: HA
authors.lastname: Alıcı
authors.affiliation: Psychiatry, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Nazan
authors.initials: N
authors.lastname: Aydin
authors.affiliation: Pathology, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Sare
authors.initials: S
authors.lastname: Altas
authors.affiliation: Histology, Medical Faculty, Ataturk University, Erzurum, Turkey.
authors.forename: Bunyami
authors.initials: B
authors.lastname: Unal
keywords: Carotid body; Glossopharyngeal nerve; Respiratory arrest; Subarachnoid hemorrhage