Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

Irikura, Katsumi; Morii, Seiji; Miyasaka, Yoshio; Yamada, Masaru; Tokiwa, Kaichi; Yada, Kenzoh

doi:10.1161/01.str.27.8.1399

Cited by 33 publications

(12 citation statements)

References 17 publications

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“…Batjer demonstrated the ability of arteries to vasodilate but an inability to vasoconstrict in response to increased pressure, a finding confirmed in a rat model [11,20,21] . We suggest that the vasoconstriction in response to SAH in our patient demonstrated that the impairment of vasoconstriction in response to elevated pressure, which has been argued to underlie NPPB syndrome, is not due to some global inability of the vasculature to constrict.…”

Section: Discussionmentioning

confidence: 76%

Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

Alexander

Connolly²,

Meyers³

2010

WJR

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Cerebral arteriovenous malformations (AVMs) have abnormally enlarged arteries and veins prone to spontaneous hemorrhage. Immediately following surgical excision of a cerebral AVM, even normal brain tissue surrounding the lesion is subject to hemorrhage, a phenomenon termed normal perfusion pressure breakthrough (NPPB) syndrome. According to this theory, arteries supplying cerebral AVMs become dilated and lose their capacity to dilate or constrict to autoregulate pressure. Acutely after removal of a cerebral AVM, excessive blood pressure in these arterial feeders can cause normal brain tissue to bleed. However, this theory remains controversial. We present a patient with a cerebral AVM that demonstrated cerebrovascular reactivity and argues against an assumption underlying the theory of NPPB syndrome.

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Section: Discussionmentioning

confidence: 76%

Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

Alexander

Connolly²,

Meyers³

2010

WJR

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“…3), helping to normalize the significant disturbances in uFA and ARA-CoA concentrations evident at 6 h (Tables 1 and 2). However, autoregulation remains abnormal and the brain is more vulnerable to additional insults such as hypotension, hypoxia and further ischemia following BCCL[62]. …”

Section: Discussionmentioning

confidence: 99%

Bilateral Common Carotid Artery Ligation Transiently Changes Brain Lipid Metabolism in Rats

et al. 2012

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Brain lipid metabolism was studied in rats following permanent bilateral common carotid artery ligation (BCCL), a model for chronic cerebral hypoperfusion. Unesterified (free) fatty acids (uFA) and acyl-CoA concentrations were measured 6 h, 24 h, and 7 days after BCCL or sham surgery, in high energy-microwaved brain. In BCCL compared to sham rats, cPLA2 immunoreactivity in piriform cortex, and concentrations of total uFA and arachidonoyl-CoA, an intermediate for arachidonic acid reincorporation into phospholipids, were increased only at 6 h. At 24 h, immunoreactivity for secretory phospholipase A2 (sPLA2), which may regulate blood flow, was increased near cortical and hippocampal blood vessels. BCCL did not affect difference brain IB4+ microglia, glial fibrillary acidic protein (GFAP)+ astrocytes, cyclooxygenase-2 (COX-2) immunoreactivity at any time, but increased cytosolic cPLA2 immunoreactivity in one region at 6 h. Thus, BCCL affected brain lipid metabolism transiently, likely because of compensatory sPLA2-mediated vasodilation, without producing evidence of neuroinflammation.

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“…Brain-derived neurotrophic factor production declines with age (Sohrabji and Lewis, 2006) and is reduced by age-dependent vascular risk factors such as hypertension (Lee et al, 2006), hypoperfusion (Irikura et al, 1996), and poor glucose metabolism (Krabbe et al, 2007). Although experimental study of BDNF effects on brain aging is hampered by impossibility to manipulate human BDNF levels in vivo , natural occurring ‘mendelian randomization’ (Katan, 1986) of individuals into groups by BDNF availability presents an opportunity for an inquiry into BDNF effects.…”

Section: Introductionmentioning

confidence: 99%

BDNF val66met polymorphism influences age differences in microstructure of the corpus callosum

Kennedy

Rodrigue

Land

et al. 2009

Front. Hum. Neurosci.

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Brain-derived neurotrophic factor (BDNF) plays an important role in neuroplasticity and promotes axonal growth, but its secretion, regulated by a BDNF gene, declines with age. The low-activity (met) allele of common polymorphism BDNF val66met is associated with reduced production of BDNF. We examined whether age-related reduction in the integrity of cerebral white matter (WM) depends on the BDNF val66met genotype. Forty-one middle-aged and older adults participated in the study. Regional WM integrity was assessed by fractional anisotropy (FA) computed from manually drawn regions of interest in the genu and splenium of the corpus callosum on diffusion tensor imaging scans. After controlling for effects of sex and hypertension, we found that only the BDNF 66met carriers displayed age-related declines in the splenium FA, whereas no age-related declines were shown by BDNF val homozygotes. No genotype-related differences were observed in the genu of the corpus callosum. This finding is consistent with a view that genetic risk for reduced BDNF affects posterior regions that otherwise are considered relatively insensitive to normal aging. Those individuals with a genetic predisposition for decreased BDNF expression may not be able to fully benefit from BDNF-based plasticity and repair mechanisms.

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Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

Cited by 33 publications

References 17 publications

Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

Bilateral Common Carotid Artery Ligation Transiently Changes Brain Lipid Metabolism in Rats

BDNF val66met polymorphism influences age differences in microstructure of the corpus callosum

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