title: The effect of degenerated neuron density of petrosal ganglion on the development of blood pressure variabilities after subarachnoid hemorrhage in a rabbit model: an experimental study.
abstract: OBJECTIVE
  The aim of this study was to determine the relationship between ischemic neurodegeneration, of the petrosal ganglion of the glossopharyngeal nerve, and BP fluctuations, after subarachnoid hemorrhage (SAH).
  
  
  METHODS
  Twenty-four rabbits had their blood pressure and heart rhythms studied daily over 20 days. Then, the histopathology of the petrosal ganglion was examined in all animals. Normal and apoptotic neuron density of the petrosal ganglion and blood pressure values were compared statistically.
  
  
  RESULTS
  Mean total volume of the petrosal ganglia was calculated as 0.9 ± 0.34/mm3. BP level of control group was 96.1 ± 2.1 mmHg; 116.5 ± 4 mmHg of mild hypertension (HT) group and 128.1 ± 3.6mmHg in the severe HT group. When the groups were compared to each other they were significantly different. The level of normal-apoptotic neuron in control group was 11,240 ± 802/mm³ -40 ± 6.3/mm³; 9730 ± 148.7/mm³ - 1560 ± 256.2/mm³ in the mild HT group and 6870 ± 378.8/mm³-4240 ± 628.2/mm³ in the severe HT group. When the groups were compared to each other there was significantly difference.
  
  
  CONCLUSIONS
  Blood pressure variability observed in this study may be explained by ischemic neurodegeneration of petrosal ganglia caused by SAH. The results of this study suggest that petrosal ganglion ischemia has potential implications for the development of hypertension. These findings suggest that new treatment strategies should be considered for the treatment of SAH.
authors.affiliation: Sisli Research and Education Hospital, Department of Neurosurgery, Istanbul Turkey.
authors.forename: Ahmet Murat
authors.initials: AM
authors.lastname: Musluman
authors.forename: Mehmet Dumlu
authors.initials: MD
authors.lastname: Aydin
authors.forename: Adem
authors.initials: A
authors.lastname: Yilmaz
authors.forename: Tufan
authors.initials: T
authors.lastname: Cansever
authors.forename: Ayhan
authors.initials: A
authors.lastname: Kanat
authors.forename: Cemal
authors.initials: C
authors.lastname: Gundogdu
authors.forename: Zeynep
authors.initials: Z
authors.lastname: Cakir
authors.forename: Mucahit
authors.initials: M
authors.lastname: Emet
authors.forename: Nesrin
authors.initials: N
authors.lastname: Gursan
authors.forename: Nazan
authors.initials: N
authors.lastname: Aydin
authors.forename: Bunyamin
authors.initials: B
authors.lastname: Unal
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D020520:Brain Infarction / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D002452:Cell Count; D002536:Cerebral Arteries / Q000294:innervation / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D017950:Ganglia, Sensory / Q000473:pathology* / Q000503:physiopathology; D005930:Glossopharyngeal Nerve / Q000473:pathology / Q000503:physiopathology; D020435:Glossopharyngeal Nerve Diseases / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D017777:Parasympathetic Fibers, Postganglionic / Q000033:anatomy & histology / Q000503:physiopathology; D011817:Rabbits; D011984:Sensory Receptor Cells / Q000473:pathology; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000503:physiopathology