Cerebral blood flow and histopathological changes following permanent bilateral carotid artery ligation in Wistar rats

Tsuchiya, Masahiko; Sako, Kazuhiro; Yura, Shigeki; Yonemasu, Yukichi

doi:10.1007/bf00229004

Cited by 134 publications

(84 citation statements)

References 18 publications

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“…Animal models offer a good possibility to reveal the potential underlying mechanisms that link reduced CBF and the decaying capillary condition in the brain. For example, the permanent ligation of both common carotid arteries of rats (two vessel occlusion, 2VO) was developed as a model of chronic cerebral hypoperfusion, where the blood supply to the brain is reduced to about 70% of the original rate [54]. This agrees with the drop in CBF in the hippocampus and temporal cortex of AD patients [13,41].…”

Section: Reduced Cbf and Cerebral Capillary Ultrastructurementioning

confidence: 85%

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Farkas

Vos

Steur

et al. 2000

Neurobiology of Aging

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Section: Reduced Cbf and Cerebral Capillary Ultrastructurementioning

confidence: 85%

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Farkas

Vos

Steur

et al. 2000

Neurobiology of Aging

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“…14,21,22 Our previous studies revealed that the WM is preferentially damaged in these rats with an increase in reactive astroglia and activated microglia and that WM lesions are found mostly in the optic nerve and optic tract and to a lesser extent in the medial part of the corpus callosum, anterior commissure, internal capsule, and caudoputamen. 10 -14 Furthermore, these animals are cognitively impaired in the Morris water maze and radial maze tasks.…”

Section: Miyamoto Et Al Neuronal Damage By Hypocapnia During Anesthesmentioning

confidence: 90%

“…The neuronal damage occurs in the gray matter, including the hippocampus, the cerebral cortex, the caudoputamen, and the ventrolateral part of the thalamus in association with reactive astrogliosis and activation of microglia in the same regions. 36 -40 Conversely, the gray matter lesions in chronic cerebral hypoperfusion are mild or scarce, 10,21,41 suggesting that regional tissue vulnerability depends on the mode of ischemic insult. Therefore, additional gray matter damage after hypocapnia, as evidenced by the loss of MAP immunoreactivity in the caudoputamen and the cerebral cortex, may indicate an overlay of acute ischemic insult onto chronic ischemic damage.…”

Section: Miyamoto Et Al Neuronal Damage By Hypocapnia During Anesthesmentioning

confidence: 99%

Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion

Miyamoto

Tomimoto

Nakao

et al. 2001

Stroke

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Background and Purpose-Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods-Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. Results-The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. Conclusions-These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia. (Stroke. 2001;32: 2920-2925.)

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“…Chronic encephalic hypoxemia in rats can be achieved by permanent bilateral carotid ligation (PBCL), which generates chronic moderate hypoglycemia that is associated with ageing and dementia, besides neurocognitive impairment and systemic reactions such as sympathetic nervous system reactions, immune cellular suppression, and opportunity for spontaneous bacterial infections [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

Autogenous fecal peritonitis in Wistar rats with permanent bilateral carotid occlusion: morbidity, mortality and microbiological response

et al. 2013

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PURPOSE:To investigate morbidity, mortality and microbiological response to fecal peritonitis induced in Wistar rats with permanent bilateral carotid ligation (PBCL). METHODS:Fecal peritonitis was induced in 30 rats, with 10 animals in each group: Group1 -normal young animals; Group2 -normal mature animals; and Group3 -rats with PBCL after four months postoperative follow-up. Peritonitis was induced with 10% stool suspension. Morbidity and mortality were evaluated. The survival animals after seven days were euthanized for tests. For microbiological studies blood were collected from the carotids and right ventricle; and fragments of lung and peritoneum. RESULTS:The morbidity and mortality of young animals were significantly lower than in mature animals with and without PBCL.There was no difference in morbidity and mortality among mature rats with and without PBCL. The diversity of microorganisms producing septicemia was similar to native micro biota of the large bowel. CONCLUSIONS:The immune response was more efficient in young animals, represented by significant less morbidity and no natural mortality. PBLC did not affect morbidity and mortality in mature rats. The immune response to fecal peritonitis has age as an independent predictor.

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Cerebral blood flow and histopathological changes following permanent bilateral carotid artery ligation in Wistar rats

Cited by 134 publications

References 18 publications

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion

Autogenous fecal peritonitis in Wistar rats with permanent bilateral carotid occlusion: morbidity, mortality and microbiological response

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