Mortality and cerebral metabolism after bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats.

Fujishima, M; Ogata, Jun; Sugi, Tomei; Omae, Teruo

doi:10.1136/jnnp.39.3.212

Cited by 53 publications

(16 citation statements)

References 22 publications

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“…5,6 throughout the experiment. Our previous studies [7][8][9][10] have demonstrated that The animals were divided into two experimental spontaneously hypertensive rats (SHR) are more sus groups: one for measurements of local CBF and the ceptible to cerebral ischemia than normotensive rats other for determinations of brain tissue metabolites. (NTR) following bilateral carotid occlusion, suggest ing that the cerebral vasoreactivities to changes of the…”

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confidence: 99%

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Ishitsuka¹,

Fujishima²,

Nakatomi³

et al. 1982

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SUMMARY Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral bloodflow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induced hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paC0 2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p < 0.05). When paCC>2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypo capnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.Stroke Vol 13, No 5, 1982 IT HAS BEEN KNOWN that hyperventilation leads to cally ventilated with a gas mixture of 70% N 2 0 and vasoconstriction of cerebral arteries with reduced cere 30% of 0 2 . One femoral artery was cannulated to bral blood flow (CBF) and cerebral oxygen tension, 1 ' 2 measure blood pressure and for anaerobic sampling of and consequently alters the brain metabolism. '• 3 4 The arterial blood for pC0 2 , p0 2 and pH determinations electroencephalographic changes during hyperventila with a Model 113 IL meter. The body temperature, tion are indistinguishable from those observed during measured in the rectum, was kept close to 37°C cerebral hypoxia. 5,6 throughout the experiment. Our previous studies 7-10 have demonstrated that The animals were divided into two experimental spontaneously hypertensive rats (SHR) are more sus groups: one for measurements of local CBF and the ceptible to cerebral ischemia than normotensive rats other for determinations of brain tissue metabolites. (NTR) following bilateral carotid occlusion, suggest ing that the cerebral vasoreactivities to changes of the Cerebral Blood Flowperfusion pressure might be different between SHR Twenty-two NTR and 22 SHR were used for this and NTR. In fact, the lower limit of cerebral autoregupurpose. The animal's head was fixed in a head holder, lation is significantly higher in SHR than NTR, and the and two small burr holes were made on the skull 2 mm increased cerebral vascular resistance due to the persis lateral to the bregma on each side for stereotaxic inser tent high blood pressure is responsible for such upward tion of teflon-coated platinum electrodes, one in the shift of the autoregulation in SHR...

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confidence: 99%

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Ishitsuka¹,

Fujishima²,

Nakatomi³

et al. 1982

Stroke

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“…1 This susceptibility is not unique to the gerbil,' since 100 percent mortality rates have been reported for other laboratory rodents subjected to bilateral carotid arterial ligation. 10 ' n It was the gerbil's special susceptibility to unilateral carotid arterial ligation, however, which led to its introduction as a useful model of cerebral ischemia. 1 '' When one carotid artery is ligated, the ipsilateral cerebral hemisphere is dependent upon the anterior communicating artery for the critical blood supply which would prevent infarction and allow the animal to survive.…”

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A gerbil model of cerebral ischemia suitable for drug evaluation.

Jarrott¹,

Domer²

1980

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SUMMARY Cerebral ischemia was produced in the Mongolian gerbil by bilateral occlusion of the carotid arteries. Although the cerebral ischemia so produced was not total, a mortality rate of 100% was obtained if the occlusion was raaintained for 60 min in gerbiis weighing 45-55 gm. Few deaths were obserred after 50 min of bilateral carotid arterial occlusion. Test drags were administered, after the removal of the arterial dips, to groups of gerbiis to determine the mortality rate associated with each drug. Isoproterenol 50 mg/kg, amphetamine 5.0 mg/kg, and methytprednisolone 35 mg/kg improved survival after cerebral ischemia. Atropine 1 mg/kg, thiosemlcarbazide 4 mg/kg, aminooxyacetic add 100 mg/kg, tbeophylline 100 mg/kg, and phenytoin 50 mg/kg were associated with a reduced survival after cerebral ischenia. The known tendency of the gerbil to exhibit spontaneous seizures and the frequency and severity of the observed post-iscbemlc seizures suggest that the lethality of prolonged cerebral ischemia may be, in part, related to seizures triggered by the cerebral ischemia.

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“…However, SHRs subjected to the bilateral CCA occlusion (SHR-2VO) have shown greater CBF reduction accompanied by more extensive cerebral infarcts and demyelinating changes and higher mortality rate (72%; 78 of 108) than the normotensive counterpart WKY rats (16%; 7 of 43). 14,15 Besides the high mortality, severe CBF reduction with marked infarctions may not adequately represent SIVD. In the current study, we tested ACs in SHRs and established the SHR-2VGO model which may more precisely mimic SIVD because of the underlying small vessel pathology.…”

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Gradual cerebral hypoperfusion in spontaneously hypertensive rats induces slowly evolving white matter abnormalities and impairs working memory

Kitamura

Saitô

Maki

et al. 2016

J Cereb Blood Flow Metab

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Rats subjected to bilateral common carotid arteries (CCAs) occlusion or 2-vessel occlusion (2VO) have been used as animal models of subcortical ischemic vascular dementia (SIVD). However, these models possess an inherent limitation in that cerebral blood flow (CBF) drops sharply and substantially after ligation of CCAs without vascular risk factors and causative small vessel changes. We previously reported a novel rat model of 2-vessel gradual occlusion (2VGO) in which ameroid constrictors (ACs) were placed bilaterally in the CCAs of Wistar-Kyoto rats. To simulate SIVD pathology more closely, we applied ACs in spontaneously hypertensive rats (SHRs), which naturally develop small vessel pathology, and compared their phenotypes with SHR-2VO and sham-operated rats. The mortality rate of the SHR-2VGO was 0% while that of the SHR-2VO was 56.5%. The CBF of the SHR-2VO dropped to 50% of the baseline level at 3 h, whereas the SHR-2VGO showed a gradual CBF reduction reaching only 68% of the baseline level at seven days. The SHR-2VGO showed slowly evolving white matter abnormalities and subsequent spatial working memory impairments of a similar magnitude to the remaining SHR-2VO at 28 days. We suggest the SHR-2VGO robustly replicates selective aspects of the pathophysiology of SIVD with low mortality rate.

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Mortality and cerebral metabolism after bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats.

Cited by 53 publications

References 22 publications

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

A gerbil model of cerebral ischemia suitable for drug evaluation.

Gradual cerebral hypoperfusion in spontaneously hypertensive rats induces slowly evolving white matter abnormalities and impairs working memory

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