Preceding functional tooth loss delays recovery from acute cerebral hypoxia and locomotor hypoactivity after murine subarachnoid haemorrhage

Mutoh, Tatsushi; Sasaki, Kazumasu; Tatewaki, Yasuko; Kunitoki, Keiko; Takano, Yoshinao; Taki, Yasuyuki

doi:10.1111/1440-1681.12874

Cited by 7 publications

(2 citation statements)

References 33 publications

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“…Studies with stroke model that analyzed the vertical and horizontal movements after brain lesion using open field test reported a reduction of locomotor activity at 3, 7, and 14 days after ischemic induction by comparing all experimental groups to basal time, but in ischemic groups the significant results indicated motor impairment deficit with habituation effect [ 52 – 54 ].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of temperature induction in focal ischemic thermocoagulation model

et al. 2018

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The thermocoagulation model, which consists of focal cerebral ischemia with craniectomy, is helpful in studying permanent ischemic brain lesions and has good reproducibility and low mortality. This study analyzed the best conditions for inducing a focal ischemic lesion by thermocoagulation. We investigated parameters such as temperature and thermal dissipation in the brain tissue during induction and analyzed real-time blood perfusion, histological changes, magnetic resonance imaging (MRI), and motor behavior in a permanent ischemic stroke model. We used three-month-old male Wistar rats, weighing 300–350 g. In the first experiment, the animals were divided into four groups (n = 5 each): one sham surgery group and three ischemic lesion groups having thermocoagulation induction (TCI) temperatures of 200°C, 300°C, and 400°C, respectively, with blood perfusion (basal and 30 min after TCI) and 2,3,5-Triphenyl-tetrazolium chloride (TTC) evaluation at 2 h after TCI. In the second experiment, five groups (n = 5 each) were analyzed by MRI (basal and 24 h after TCI) and behavioral tests (basal and seven days after TCI) with the control group added for the surgical effects. The MRI and TTC analyses revealed that ischemic brain lesions expressively evolved, especially at TCI temperatures of 300°C and 400°C, and significant motor deficits were observed as the animals showed a decrease frequency of movement and an asymmetric pattern. We conclude that a TCI temperature of 400°C causes permanent ischemic stroke and motor deficit.

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Section: Discussionmentioning

confidence: 99%

Evaluation of temperature induction in focal ischemic thermocoagulation model

et al. 2018

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“…17 Figure S1a). 10,11,21 A 3D reconstructed vascularity of the flow signals was then acquired with the power Doppler mode ( Figure S1b) to calculate %vascularity 22 within the scanned brain volume (step size of 0.2 mm for ±15 coronal slices from the level of basal ganglia; scan time: 7 minutes 21 seconds) using an offline analysis software. Reference CBF was measured using a laser Doppler probe, and the values were normalized relative to baseline for each animal.…”

Section: Materials S and Me Thodsmentioning

confidence: 99%

Non‐invasive three‐dimensional power Doppler imaging for the assessment of acute cerebral blood flow alteration in a mouse model of subarachnoid haemorrhage

Yamamoto

Mutoh

Sasaki

et al. 2018

Clin Exp Pharma Physio

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Subarachnoid haemorrhage (SAH) is the leading cause of acute death and permanent disability in people suffering stroke worldwide. 1 Clinical and laboratory investigations have shown that early brain injury (EBI) is closely linked to poor outcomes and the development of delayed cerebral ischaemia in patients after SAH. 2,3 Cerebral blood flow (CBF) autoregulation can be impaired by a wide variety of pathological conditions including post-SAH EBI. For preclinical studies, visualization of anatomy and functional processes is mandatory. Although there are many neuroimaging techniques (eg, magnetic resonance imaging [MRI], single-photon emission computed tomography [SPECT], positron-emission tomography [PET], two-photon excitation laser microscopy, laser speckle and photoacoustic imaging), 4-13 these can suffer from limitations in resolution, insufficient depth, the use of ionizing radiation or expense. High-frequency ultrasound can provide real-time microvascular information noninvasively with high spatiotemporal resolution.With the recent advancement in three-dimensional (3D) power Doppler ultrasound technology, quantitative 3D analysis in the assessment of the vascularization of tumour tissues and foetal brain has become feasible. 14,15 This in vivo study aimed to validate the feasibility of 3D power Doppler-based analysis of CBF during the acute phase of experimental SAH in mice, compared with conventional measurements. | RE SULTSA total of 25 mice were subjected to SAH by endovascular perforation; 3 (12%) were scored as grade 1, 2 (8%) as grade 2, 11 (44%) as grade 3, and 9 (36%) as grade 4, according to the MRI grading scale. 16,17 Acute infarction was detected in three mice (grade 3 in two mice and grade 4 in one) by diffusion-weighted MRI on day 1.Global depression of 3D reconstructed CBF signals within the scanned brain area (±6 mm coronal slices from the level of the basal ganglia) was notable early (~24 hours) after SAH induction (P < 0.001; one-way analysis of variance [ANOVA] and Bonferroni post hoc test) ( Figure S1). This depression recovered to close to the baseline level SummaryWe aimed to evaluate the feasibility of a non-invasive method of cerebral blood flow (CBF) measurement using high-frequency power Doppler ultrasound imaging in a mouse model of subarachnoid haemorrhage (SAH). The 3-dimensionally (3D) reconstructed blood flow signals (%vascularity) within the brain volume of the middle cerebral artery territory correlated well with reference parameters, baseline carotid artery blood flow (r 2 = 0.52, P < 0.0001) and normalized CBF changes (r 2 = 0.74 P < 0.0001). These data suggest that the 3D power Doppler analysis may have the potential for reflecting real-time CBF changes during the acute phase of experimental SAH, which may be applicable to preclinical studies on early brain injury. K E Y W O R D Scerebral blood flow, mouse model, subarachnoid haemorrhage, ultrasound imaging

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