Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

Wei, Ling; Lin, Shinn Zong; Tajima, Atsushi; Nakata, Hiroyuki; Acuff, V.; Patlak, Clifford S.; Pettigrew, Karen D.; Fenstermacher, Joseph D.

doi:10.1161/01.hyp.20.4.501

Cited by 42 publications

(35 citation statements)

References 24 publications

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“…14 At the end of the experimental period, the rats were decapitated. Immediately the brain was rapidly removed and instantly frozen in 2-methylbutane previously cooled to -45°C.…”

Section: Measurements Of Brain Volumes and Thicknessmentioning

confidence: 99%

“…Sections designated for histology were placed on glass slides, dried at 45°C, stained with cresyl violet, and covered. Sets of histological sections from 10 of the 12 SHR and 10 of the 12 WKY rats from the study of Wei et al 14 were selected for volume and thickness measurements. The sets selected were the ones that provided the most sections of the entire brain and the areas of interest.…”

Section: Measurements Of Brain Volumes and Thicknessmentioning

confidence: 99%

“…13 At 6-7 months of age, however, LCGU appears to be lower in most gray matter areas of SHR relative to WKY rats. 14 These LCGU findings indicate that function is altered in many parts of the nervous system of young adult SHR, including a number of structures that have little or no role in sympathetic nervous system activity and blood pressure regulation. The brain of the young adult SHR, thus, seems to differ both morphologically and physiologically from that of the WKY, and these differences appear to involve many parts of the nervous system.…”

mentioning

confidence: 95%

“…The purpose of the present study was to test the hypothesis that the structure of many brain areas differs between 6-7-month-old SHR and WKY rats by using histological sections obtained from previously published work. 1415 With freeze-fixed sections, 14 the volume of the ventricular system, the entire brain, six specific gray matter structures, and two white matter areas plus the thickness of two cortical regions were estimated. The frequency of neuronal nuclei in nine brain areas was determined on the perfusion-fixed histological samples.…”

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confidence: 99%

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Smaller local brain volumes and cerebral atrophy in spontaneously hypertensive rats.

et al. 1993

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Spontaneously hypertensive rats (SHR) have enlarged cerebral ventricles from 8 weeks of age onward and smaller brains than age-matched, normotensive Wistar-Kyoto (WKY) rats (controls). At 6-7 months of age local cerebral glucose utilization is apparently lower in many brain areas of SHR relative to WKY rats. These observations led to the hypothesis that there are morphological differences between these two strains of rats in many, if not all, brain areas. This hypothesis was tested in 6-7-month-old SHR and WKY rats by quantitating 1) the volumes of the ventricular system, whole brain, six gray matter structures, and two white matter areas; 2) the thickness of two regions of the cerebral cortex; and 3) the frequency of neuronal nuclei (neuronal frequency) in nine brain areas. Ventricular volume was twofold greater in SHR than in control rats. The volumes of the entire brain and all six gray matter structures plus the thickness of the two cortical regions were 11-25% less in SHR. Neuronal frequency was, however, similar in the two rat strains. The latter finding coupled with the smaller regional tissue volumes indicates appreciably fewer neurons per brain structure in young adult SHR than in controls. These results indicate significant cerebral structural differences between young adult SHR and WKY rats and suggest that structure as well as metabolism are abnormal in the SHR brain. is not only hypertensive but also hyperactive 2 " 4 and hydrocephalic. 5 -7 Relative to age-and sex-matched Wistar-Kyoto (WKY) rats, the normotensive control strain for SHR, total brain weight and volume are about 11% less in 12-week-old male SHR.8 For 8-month-old animals, Lehr et al 9 have reported that the midbrain and diencephalon are smaller and the pons is larger in SHR than WKY rats. Of relevance to these observations, magnetic resonance imaging has indicated that brain volume is reduced and ventricular volume is greater in humans with essential hypertension than in agematched control subjects. 10Local cerebral glucose utilization (LCGU) is highly dependent on local neural activity, is commonly used as an indicator of the functional state of cerebral tissue, and varies appreciably among brain areas and conditions.11 -13 For most brain structures, LCGU is virtually the same in 11-12-week-old SHR and WKY rats, but for the superior cervical, cardiac, and coeliac sympathetic ganglia, LCGU is significantly less in SHR than in WKY rats.13 At 6-7 months of age, however, LCGU

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“…14 At the end of the experimental period, the rats were decapitated. Immediately the brain was rapidly removed and instantly frozen in 2-methylbutane previously cooled to -45°C.…”

Section: Measurements Of Brain Volumes and Thicknessmentioning

confidence: 99%

Section: Measurements Of Brain Volumes and Thicknessmentioning

confidence: 99%

mentioning

confidence: 95%

mentioning

confidence: 99%

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Smaller local brain volumes and cerebral atrophy in spontaneously hypertensive rats.

et al. 1993

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“…§ During sensory stimulation these increments generally are small in awake humans (10) and animals (11), with a maximum increase of about 40% for intense stimulations (12,13). Increments of about 10% are more usual during physiological visual stimuli (14,15) or cognitive tasks (16).…”

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Stimulated changes in localized cerebral energy consumption under anesthesia

Shulman

Rothman²,

Hyder³

1999

Proc. Natl. Acad. Sci. U.S.A.

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Focal changes in the cerebral metabolic rate of glucose utilization (CMR glc ) are small (10-40%) during sensory activation in awake humans, as well as in awake rodents and primates (20-50%). They are significantly larger (50-250%) in sensory activation studies of anesthetized rats and cats. Our data, in agreement with literature values, show that in the resting anesthetized state values of CMR glc are lower than in the resting nonanesthetized state whereas the final state values, reached upon activation, are similar for the anesthetized and nonanesthetized animals. The lower resting anesthetized state values of CMR glc explain why the increments upon activation from anesthesia are larger than when starting from the nonanesthetized conditions. Recent 13 C NMR measurements in our laboratory have established a quantitative relationship between the energetics of glucose oxidation, CMR glc (oxidative), and the f lux of the glutamate͞ ␥-aminobutyric acid͞glutamine neurotransmitter cycle, V cycle . In both the resting awake value of CMR glc (oxidative), and its increment upon stimulation, a large majority (Ϸ80%) of the brain energy consumption is devoted to V cycle . In the differencing methods of functional imaging, it is assumed that the incremental change in the measured signal represents the modular activity that supports the functional response. However, the same amount of activity must be present during the response to stimulation, irrespective of the initial basal state of the cortex. Thus, whereas the incremental signals of ⌬CMR glc can localize neurotransmitter activity, the magnitude of such activity during the response is represented by the total localized CMR glc , not the increment.Modern imaging methods detect regional changes in functional brain activity by assuming coupling between brain glucose metabolism and the underlying neuronal activity. The principle that the rate of glucose metabolism in the brain reflects functional activity was first expressed by Roy and Sherrington in 1890 (1). Since that time, there has been great progress in understanding the neuronal processes that support brain function such as action potentials and neurotransmitter action (2-4), but understanding of the coupling between these cellular processes and glucose metabolism has been limited (5). Only recently has there been evidence for a stoichiometric relationship between glucose oxidation and functional neuronal processes, in particular, to neurotransmitter fluxes (6).For a variety of technical reasons, functional metabolic imaging measures increments in regional brain glucose metabolism in response to peripheral stimulation. § During sensory stimulation these increments generally are small in awake humans (10) and animals (11), with a maximum increase of about 40% for intense stimulations (12, 13). Increments of about 10% are more usual during physiological visual stimuli (14, 15) or cognitive tasks (16). The focus on incremental glucose metabolism has led to the prevailing view in the field that the increment repr...

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A unifying hypothesis of Alzheimer's disease. III. Risk factors

Heininger

2000

Hum. Psychopharmacol. Clin. Exp.

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Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.

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Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

Cited by 42 publications

References 24 publications

Smaller local brain volumes and cerebral atrophy in spontaneously hypertensive rats.

Smaller local brain volumes and cerebral atrophy in spontaneously hypertensive rats.

Stimulated changes in localized cerebral energy consumption under anesthesia

A unifying hypothesis of Alzheimer's disease. III. Risk factors

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