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Preceding functional tooth loss delays recovery from acute cerebral hypoxia and locomotor hypoactivity after murine subarachnoid haemorrhage
Author(s) -
Mutoh Tatsushi,
Sasaki Kazumasu,
Tatewaki Yasuko,
Kunitoki Keiko,
Takano Yumi,
Taki Yasuyuki
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12874
Subject(s) - medicine , hypoactivity , anesthesia , hypoxia (environmental) , subarachnoid hemorrhage , masticatory force , chemistry , organic chemistry , oxygen , orthodontics
Summary Tooth loss and related changes in the functionality may lead to worse outcome of stroke patients, but the effect on hemorrhagic stroke remains unclear. This study aimed to determine the impact of impaired masticatory function on acute cerebral oxygenation and locomotor activity after experimental subarachnoid haemorrhage ( SAH ). Twenty C57 BL /6 mice with (MC‐treated group) or without (control group) prior treatment of cutting off the upper molars were subjected to SAH by endovascular perforation. Grading of SAH and acute cerebral infarction were assessed by MR images. Brain tissue oxygen saturation (SbtO 2 ) by photoacoustic imaging and parameters related to locomotor activity by open‐field test were analyzed serially after SAH . In all mice, global SbtO2 depression was notable immediately after SAH induction ( P <.001), which recovered close to the baseline levels until day 3. However, MC‐treated mice demonstrated a prolonged relative cerebral hypoxia (<40% of the baseline SbtO2) as compared to the control (3 ± 1 vs 1 ± 1 days; P <.05). The average distance travelled on day 7 and the ratio of central‐area distance/total travelled distance by open‐field test between days 7 and 14 were significantly lower in MC‐treated mice than in the control mice ( P <.05), although the occurrences of new infarction were not statistically different ( P >.05). These data suggest a possible link between preceding masticatory impairment and early brain injury to deteriorate neurobehavioural function in patients after SAH .