TY - JOUR
T1 - Preceding functional tooth loss delays recovery from acute cerebral hypoxia and locomotor hypoactivity after murine subarachnoid haemorrhage
AU - Mutoh, Tatsushi
AU - Sasaki, Kazumasu
AU - Tatewaki, Yasuko
AU - Kunitoki, Keiko
AU - Takano, Yumi
AU - Taki, Yasuyuki
N1 - Funding Information:
The authors thank Dr. Ikuho Kojima (Tohoku University Graduate School of Dentistry) for dental procedure instructions and Dr. Yoshi-haru Tsuru (Primetech Life Science Laboratory, Graduate School of Agricultural and Life Sciences, The University of Tokyo) for data acquisition and image analysis.
Publisher Copyright:
© 2017 John Wiley & Sons Australia, Ltd
PY - 2018/4
Y1 - 2018/4
N2 - 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 C57BL/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.
AB - 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 C57BL/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.
KW - cerebral oxygenation
KW - early brain injury
KW - mastication
KW - mouse model
KW - neurobehavioural function
KW - subarachnoid haemorrhage
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U2 - 10.1111/1440-1681.12874
DO - 10.1111/1440-1681.12874
M3 - Article
C2 - 29044603
AN - SCOPUS:85037998258
SN - 0305-1870
VL - 45
SP - 344
EP - 348
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
IS - 4
ER -