scholarly journals Diverse Functions of Pericytes in Cerebral Blood Flow Regulation and Ischemia

2015 ◽  
Vol 35 (6) ◽  
pp. 883-887 ◽  
Author(s):  
Francisco Fernandez-Klett ◽  
Josef Priller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Neuronal Activity ◽  
Flow Regulation ◽  
Functional Hyperemia ◽  
Mural Cells ◽  
Ischemic Tissue ◽  
The Brain

Pericytes are mural cells with contractile properties. Here, we provide evidence that microvascular pericytes modulate cerebral blood flow in response to neuronal activity (‘functional hyperemia’). Besides their role in neurovascular coupling, pericytes are responsive to brain damage. Cerebral ischemia is associated with constrictions and death of capillary pericytes, followed by fibrotic reorganization of the ischemic tissue. The data suggest that precapillary arterioles and capillaries are major sites of hemodynamic regulation in the brain.

Cerebral Blood Flow

PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1013-1013
Author(s):  
BARRY G. BAYLEN ◽  
GEORGE C. EMMANOUILIDES
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Patent Ductus Arteriosus ◽  
Brain Damage ◽  
Pulsatility Index ◽  
Ductus Arteriosus ◽  
Before And After ◽  
The Brain ◽  
Patent Ductus

In the commentary, "Pulsatility Index, Patent Ductus Arteriosus, and Brain Damage," It was stated that we have shown that "blood flow" to the brain was not reduced in premature lambs with left-right ductal shunting. The abstracted data referred primarily to alteration of the percent distribution of blood flow and not to changes of absolute blood flow to systemic organs before and after patent ductus arteriosus (PDA) occlusion in preterm lambs. We subsequently demonstrated that absolute cerebral blood flow (milliliters per gram per minute) in fact was significantly reduced in preterm lambs with PDA.

scholarly journals Nitric Oxide Pathways in Neurovascular Coupling Under Normal and Stress Conditions in the Brain: Strategies to Rescue Aberrant Coupling and Improve Cerebral Blood Flow

2021 ◽  
Vol 12 ◽  
Author(s):  
Cátia F. Lourenço ◽  
João Laranjinha
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nmda Receptor ◽  
Neuronal Activity ◽  
Energy Requirements ◽  
Neuronal Dysfunction ◽  
No Bioavailability ◽  
The Brain

The brain has impressive energy requirements and paradoxically, very limited energy reserves, implying its huge dependency on continuous blood supply. Aditionally, cerebral blood flow must be dynamically regulated to the areas of increased neuronal activity and thus, of increased metabolic demands. The coupling between neuronal activity and cerebral blood flow (CBF) is supported by a mechanism called neurovascular coupling (NVC). Among the several vasoactive molecules released by glutamatergic activation, nitric oxide (•NO) is recognized to be a key player in the process and essential for the development of the neurovascular response. Classically, •NO is produced in neurons upon the activation of the glutamatergic N-methyl-D-aspartate (NMDA) receptor by the neuronal isoform of nitric oxide synthase and promotes vasodilation by activating soluble guanylate cyclase in the smooth muscle cells of the adjacent arterioles. This pathway is part of a more complex network in which other molecular and cellular intervenients, as well as other sources of •NO, are involved. The elucidation of these interacting mechanisms is fundamental in understanding how the brain manages its energy requirements and how the failure of this process translates into neuronal dysfunction. Here, we aimed to provide an integrated and updated perspective of the role of •NO in the NVC, incorporating the most recent evidence that reinforces its central role in the process from both viewpoints, as a physiological mediator and a pathological stressor. First, we described the glutamate-NMDA receptor-nNOS axis as a central pathway in NVC, then we reviewed the link between the derailment of the NVC and neuronal dysfunction associated with neurodegeneration (with a focus on Alzheimer’s disease). We further discussed the role of oxidative stress in the NVC dysfunction, specifically by decreasing the •NO bioavailability and diverting its bioactivity toward cytotoxicity. Finally, we highlighted some strategies targeting the rescue or maintenance of •NO bioavailability that could be explored to mitigate the NVC dysfunction associated with neurodegenerative conditions. In line with this, the potential modulatory effects of dietary nitrate and polyphenols on •NO-dependent NVC, in association with physical exercise, may be used as effective non-pharmacological strategies to promote the •NO bioavailability and to manage NVC dysfunction in neuropathological conditions.

Hippocampal functional hyperemia mediated by NMDA receptor/NO signaling in rats during mild exercise

2012 ◽  
Vol 112 (1) ◽  
pp. 197-203 ◽  
Author(s):  
Takeshi Nishijima ◽  
Masahiro Okamoto ◽  
Takashi Matsui ◽  
Ichiro Kita ◽  
Hideaki Soya
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nmda Receptor ◽  
Neuronal Activity ◽  
Treadmill Running ◽  
Functional Hyperemia ◽  
Neuronal Activation ◽  
Metabotropic Glutamate ◽  
Group I ◽  
No Signaling

Current studies have demonstrated that exercise increases regional cerebral blood flow (rCBF), an index of neuronal activity. However, neuronal regulation of the increased rCBF in the brain parenchyma is poorly understood. We developed a running model with rats for monitoring hippocampal cerebral blood flow (Hip-CBF) and found that mild treadmill running increases Hip-CBF in a tetrodotoxin-dependent manner, suggesting that functional hyperemia, an increase in rCBF in response to neuronal activation, occurs in the running rat's hippocampus (Nishijima T and Soya H. Neurosci Res 54: 186–191, 2006). To further support our hypothesis, it was important to discover the neurogenic pathways behind the increase in Hip-CBF that occurred during running. Here, we examine the possible role of N-methyl-d-aspartate (NMDA) receptor/nitric oxide (NO) signaling and group I metabotropic glutamate receptors in mediating the Hip-CBF increase. Hip-CBF during running was measured by laser-Doppler flowmetry. Intrahippocampal drug administration was performed by microdialysis. Mild treadmill running (10 m/min) increased Hip-CBF, which was remarkably attenuated by either NMDA receptor antagonists (1 mM MK-801) or NO synthase inhibitors (2 mM NG-nitro-l-arginine methyl ester). However, group I metabotropic glutamate receptor antagonists {1 mM 7-(hydroxyimino)cyclopropa[ b]chromen-1a-carboxylate ethyl ester + 1 mM 2-methyl-6-(phenylethynyl)pyridine hydrochloride} augmented the running-induced Hip-CBF increase. We also found that rCBF in the olfactory bulb was unchanged with running. These results strongly suggest that Hip-CBF during mild exercise is regulated locally under hippocampal neuronal activity, mediated mainly through NMDA receptor/NO signaling. Collectively, these results, together with our previous findings, support our hypothesis that mild exercise elicits neuronal activation, which then triggers functional hyperemia in the rat hippocampus.

Differences in critical cerebral blood flow with age in swine

1991 ◽  
Vol 75 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Jun Harada ◽  
Akira Takaku ◽  
Shunro Endo ◽  
Naoya Kuwayama ◽  
Osamu Fukuda
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Content Type ◽  
Neonatal Pigs ◽  
S 100 ◽  
Newborn Pigs ◽  
Electroencephalogram Eeg ◽  
The Brain ◽  
Fine Print

✓ Normal cerebral blood flow (CBF), critical CBF at a flat reading of the electroencephalogram (EEG), and reversibility of the flat EEG after reperfusion were investigated in a total of 59 pigs, including seven newborns (1 to 3 days of age), 38 juveniles (1 month old), and 14 adults (7 months old). The CBF was determined by the hydrogen clearance method; the EEG was recorded continuously and a power spectrum analysis was performed. Cerebral ischemia was produced by occlusion of both common carotid arteries and induction of hypotension (approximately 50 mm Hg). The flat EEG reversibility was investigated for 3 hours after reperfusion. As parameters of brain development, the neuronal density and the time at which the S-100 protein appeared in the brain were examined. Normal CBF was highest in neonatal pigs and decreased with age. The critical CBF at a flat EEG was lowest in newborn pigs and was elevated with development of the brain. Tolerance against cerebral ischemia was greatest in newborn pigs.

Hyperthermia-induced vasoconstriction of the carotid artery, a possible causative factor of heatstroke

2004 ◽  
Vol 96 (5) ◽  
pp. 1875-1878 ◽  
Author(s):  
Seham Mustafa ◽  
O. Thulesius ◽  
H. N. Ismael
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Brain Damage ◽  
Experimental Studies ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Basal Tone

Clinical and experimental studies indicate that hyperthermia can cause heatstroke with cerebral ischemia and brain damage. However, no study has examined the direct effects of heating carotid artery smooth muscle and tested the hypothesis that hyperthermia induces arterial vasoconstriction and, thereby, decreases cerebral blood flow. We recorded isometric tension of rabbit carotid artery strips in organ baths during stepwise temperature elevation. The heating responses were tested at basal tone, in norepinephrine- and KCl-precontracted vessels, and after electrical field stimulation. Stepwise heating from 37°C to 47°C induced reproducible graded contraction proportional to temperature. The responses could be elicited at basal tone and in precontracted vessels. Heating decreased the contractile responses to norepinephrine and electrical field stimulation but increased contraction to KCl. These responses were not eliminated by pretreatment with the neuronal blocker tetrodotoxin. Our results demonstrate that heating carotid artery preparations above 37°C (normothermia) induced a reversible graded vasoconstriction proportional to temperature. In vivo this reaction may lead to a decrease in cerebral blood flow and cerebral ischemia with brain damage as in heatstroke. The heating-induced contraction is not mediated by a neurogenic process but is due to altered transcellular Ca2+ transport. Cooling, in particular of the neck area, therefore, should be used in the treatment of heatstroke.

Aging reduces cerebral blood flow regulation following an acute hypertensive stimulus

2020 ◽  
Vol 128 (5) ◽  
pp. 1186-1195
Author(s):  
Alexander J. Rosenberg ◽  
Elizabeth C. Schroeder ◽  
Georgios Grigoriadis ◽  
Sang Ouk Wee ◽  
Kanokwan Bunsawat ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Regulation ◽  
Blood Velocity ◽  
Elevated Blood ◽  
Blood Flow Regulation ◽  
Stimulus Effects ◽  
Cerebral Blood Velocity ◽  
Blood Pressure Responses ◽  
The Brain

Reductions in cerebral blood flow and increases in flow pulsatility with aging are associated to cerebrovascular disease; however, little is known about how an acute hypertensive stimulus effects cerebral blood flow regulation in an aged population. Following the hypertensive stimulus, older adults elicit an attenuated increase in cerebral blood velocity and greater transmission of pulsatile velocity to the brain compared with young adults, demonstrating reduced cerebral blood flow regulation to elevated blood pressure responses with aging.

Vorläufige Ergebnisse von 99mTc-HMPAO-SPECT-Untersuchungen bei endogenen Psychosen

1989 ◽  
Vol 28 (03) ◽  
pp. 88-91
Author(s):  
J. Schröder ◽  
H. Henningsen ◽  
H. Sauer ◽  
P. Georgi ◽  
K.-R. Wilhelm
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regions Of Interest ◽  
Post Mortem ◽  
Regional Cerebral Blood ◽  
Hmpao Spect ◽  
Endogenous Psychoses ◽  
The Brain ◽  
99Mtc Hmpao

18 psychopharmacologically treated patients (7 schizophrenics, 5 schizoaffectives, 6 depressives) were studied using 99mTc-HMPAO-SPECT of the brain. The regional cerebral blood flow was measured in three transversal sections (infra-/supraventricular, ventricular) within 6 regions of interest (ROI) respectively (one frontal, one parietal and one occipital in each hemisphere). Corresponding ROIs of the same section in each hemisphere were compared. In the schizophrenics there was a significantly reduced perfusion in the left frontal region of the infraventricular and ventricular section (p < 0.02) compared with the data of the depressives. The schizoaffectives took an intermediate place. Since the patients were treated with psychopharmaca, the result must be interpreted cautiously. However, our findings seem to be in accordance with post-mortem-, CT- and PET-studies presented in the literature. Our results suggest that 99mTc-HMPAO-SPECT may be helpful in finding cerebral abnormalities in endogenous psychoses.

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