scholarly journals Neural Vascular Mechanism for the Cerebral Blood Flow Autoregulation after Hemorrhagic Stroke

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Ming Xiao ◽  
Qiang Li ◽  
Hua Feng ◽  
Le Zhang ◽  
Yujie Chen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Hemorrhagic Stroke ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Blood Gases ◽  
Metabolic Demand ◽  
Metabolic Substrates ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation

During the initial stages of hemorrhagic stroke, including intracerebral hemorrhage and subarachnoid hemorrhage, the reflex mechanisms are activated to protect cerebral perfusion, but secondary dysfunction of cerebral flow autoregulation will eventually reduce global cerebral blood flow and the delivery of metabolic substrates, leading to generalized cerebral ischemia, hypoxia, and ultimately, neuronal cell death. Cerebral blood flow is controlled by various regulatory mechanisms, including prevailing arterial pressure, intracranial pressure, arterial blood gases, neural activity, and metabolic demand. Evoked by the concept of vascular neural network, the unveiled neural vascular mechanism gains more and more attentions. Astrocyte, neuron, pericyte, endothelium, and so forth are formed as a communicate network to regulate with each other as well as the cerebral blood flow. However, the signaling molecules responsible for this communication between these new players and blood vessels are yet to be definitively confirmed. Recent evidence suggested the pivotal role of transcriptional mechanism, including but not limited to miRNA, lncRNA, exosome, and so forth, for the cerebral blood flow autoregulation. In the present review, we sought to summarize the hemodynamic changes and underline neural vascular mechanism for cerebral blood flow autoregulation in stroke-prone state and after hemorrhagic stroke and hopefully provide more systematic and innovative research interests for the pathophysiology and therapeutic strategies of hemorrhagic stroke.

scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

Melatonin improves cerebral circulation security margin in rats

1998 ◽  
Vol 275 (1) ◽  
pp. H139-H144 ◽  
Author(s):  
Olivier Régrigny ◽  
Philippe Delagrange ◽  
Elizabeth Scalbert ◽  
Jeffrey Atkinson ◽  
Isabelle Lartaud-Idjouadiene
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Pressure Level ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation

Because melatonin is a cerebral vasoconstrictor agent, we tested whether it could shift the lower limit of cerebral blood flow autoregulation to a lower pressure level, by improving the cerebrovascular dilatory reserve, and thus widen the security margin. Cerebral blood flow and cerebrovascular resistance were measured by hydrogen clearance in the frontal cortex of adult male Wistar rats. The cerebrovasodilatory reserve was evaluated from the increase in the cerebral blood flow under hypercapnia. The lower limit of cerebral blood flow autoregulation was evaluated from the fall in cerebral blood flow following hypotensive hemorrhage. Rats received melatonin infusions of 60, 600, or 60,000 ng ⋅ kg−1 ⋅ h−1, a vehicle infusion, or no infusion ( n= 9 rats per group). Melatonin induced concentration-dependent cerebral vasoconstriction (up to 25% of the value for cerebrovascular resistance of the vehicle group). The increase in vasoconstrictor tone was accompanied by an improvement in the vasodilatory response to hypercapnia (+50 to +100% vs. vehicle) and by a shift in the lower limit of cerebral blood flow autoregulation to a lower mean arterial blood pressure level (from 90 to 50 mmHg). Because melatonin had no effect on baseline mean arterial blood pressure, the decrease in the lower limit of cerebral blood flow autoregulation led to an improvement in the cerebrovascular security margin (from 17% in vehicle to 30, 55, and 55% in the low-, medium-, and high-dose melatonin groups, respectively). This improvement in the security margin suggests that melatonin could play an important role in the regulation of cerebral blood flow and may diminish the risk of hypoperfusion-induced cerebral ischemia.

scholarly journals Corrigendum

2016 ◽  
Vol 36 (2) ◽  
pp. 456-456
Keyword(s):  
Blood Flow ◽  
Cell Death ◽  
Cerebral Blood Flow ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Pyroptotic neuronal cell death mediated by the AIM2 inflammasome Adamczak SE, de Rivero Vaccari JP, Dale G, Brand FJ 3rd, Nonner D, Bullock MR, Dahl GP, Dietrich WD, Keane RW Journal of Cerebral Blood Flow & Metabolism 2014; 34: 621–629 .

scholarly journals REGULATION OF CEREBRAL BLOOD FLOW IN HUMANS: PHYSIOLOGY AND CLINICAL IMPLICATIONS OF AUTOREGULATION

2021 ◽  
Author(s):  
Jurgen A.H.R. Claassen ◽  
Dick H.J. Thijssen ◽  
Ronney B Panerai ◽  
Frank M. Faraci
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Function ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Blood Gases ◽  
Clinical Implications ◽  
Arterial Blood ◽  
The Impact

Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste. This matching requires continuous regulation of cerebral blood flow (CBF), which can be categorized into four broad topics: 1) autoregulation, which describes the response of the cerebrovasculature to changes in perfusion pressure, 2) vascular reactivity to vasoactive stimuli [including carbon dioxide (CO2)], 3) neurovascular coupling (NVC), i.e., the CBF response to local changes in neural activity (often standardized cognitive stimuli in humans), and 4) endothelium-dependent responses. This review focuses primarily on autoregulation and its clinical implications. To place autoregulation in a more precise context, and to better understand integrated approaches in the cerebral circulation, we also briefly address reactivity to CO2 and NVC. In addition to our focus on effects of perfusion pressure (or blood pressure), we describe the impact of select stimuli on regulation of CBF (i.e., arterial blood gases, cerebral metabolism, neural mechanisms, and specific vascular cells), the inter-relationships between these stimuli, and implications for regulation of CBF at the level of large arteries and the microcirculation. We review clinical implications of autoregulation in aging, hypertension, stroke, mild cognitive impairment, anesthesia, and dementias. Finally, we discuss autoregulation in the context of common daily physiological challenges, including changes in posture (e.g., orthostatic hypotension, syncope) and physical activity.

Alteration of pial vessel responses to blood pressure changes in rats after hypoxia

1987 ◽  
Vol 65 (11) ◽  
pp. 2265-2268 ◽  
Author(s):  
B. Y. Ong ◽  
J. J. Kettler ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pial Arteries ◽  
Similar Time ◽  
Vascular Responses ◽  
Cranial Window ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation ◽  
Pial Vessel

Previous studies in newborn lamb have shown impairment of cerebral blood flow autoregulation after hypoxia followed by reoxygenation. The present study was done to see if such a phenomenon existed in the adult rat and if it could be demonstrated at the level of the pial arterioles. Using an open cranial window preparation, we assessed the changes in pial vessel diameter during blood pressure alterations induced by hemorrhage and reinfusion of blood, before and after 30 s of hypoxia, in 15 male Sprague–Dawley rats. Mean diameters of pial arteries in the study group of rats were 128 ± 54 μm before hypoxia and 141 ± 61 μm after normoxia following hypoxia. The corresponding diameters in rats serving as time controls were 136 ± 52 and 138 ± 52 μm. Slopes of pial vessel diameters as a function of mean arterial blood pressures descreased significantly (p < 0.05) after hypoxia from −0.86 ± 0.45 to 0.03 ± 0.66 (mean ± SD). In the control rats not subjected to hypoxia, the slopes remained unchanged over a similar time period (−0.60 ± 0.16 and −0.42 ± 0.19). The negative slopes indicate that pial vessels dilate during hypotension and constrict during hypertension. Such vascular responses may play a role in autoregulation of cerebral blood flow. We found that a relatively brief period of hypoxia can cause a long-lasting impairment of vascular responses even after restoration of normoxia. These findings are consistent with a previous report of persistent impairment of cerebral blood flow autoregulation after a brief period of hypoxia.

Cerebral blood flow autoregulation in early experimental S. pneumoniae meningitis

2007 ◽  
Vol 102 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Michael Pedersen ◽  
Christian T. Brandt ◽  
Gitte M. Knudsen ◽  
Christian Østergaard ◽  
Peter Skinhøj ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Intracisternal Injection ◽  
Cerebral Blood Flow Autoregulation

We studied cerebral blood flow (CBF) autoregulation and intracranial pressure (ICP) during normo- and hyperventilation in a rat model of Streptococcus pneumoniae meningitis. Meningitis was induced by intracisternal injection of S. pneumoniae. Mean arterial blood pressure (MAP), ICP, cerebral perfusion pressure (CPP, defined as MAP − ICP), and laser-Doppler CBF were measured in anesthetized infected rats ( n = 30) and saline-inoculated controls ( n = 30). CPP was either incrementally reduced by controlled hemorrhage or increased by intravenous norepinephrine infusion. Twelve hours postinoculation, rats were studied solely during normocapnia, whereas rats studied after 24 h were exposed to either normocapnia or to acute hypocapnia. In infected rats compared with control rats, ICP was unchanged at 12 h but increased at 24 h postinoculation (not significant and P < 0.01, respectively); hypocapnia did not lower ICP compared with normocapnia. Twelve hours postinoculation, CBF autoregulation was lost in all infected rats but preserved in all control rats ( P < 0.01). Twenty-four hours after inoculation, 10% of infected rats had preserved CBF autoregulation during normocapnia compared with 80% of control rats ( P < 0.01). In contrast, 60% of the infected rats and 100% of the control rats showed an intact CBF autoregulation during hypocapnia ( P < 0.05 for the comparison of infected rats at normocapnia vs. hypocapnia). In conclusion, CBF autoregulation is lost both at 12 and at 24 h after intracisternal inoculation of S. pneumoniae in rats. Impairment of CBF autoregulation precedes the increase in ICP, and acute hypocapnia may restore autoregulation without changing the ICP.

scholarly journals Role of cerebral blood flow in extreme breath holding

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anthony R. Bain ◽  
Philip N. Ainslie ◽  
Ryan L. Hoiland ◽  
Chris K. Willie ◽  
David B. MacLeod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oral Administration ◽  
Blood Gases ◽  
Breath Holding ◽  
Breath Hold ◽  
Cyclooxygenase Inhibitor ◽  
Arterial Blood Gases ◽  
Arterial Blood

AbstractThe role of cerebral blood flow (CBF) on a maximal breath-hold (BH) in ultra-elite divers was examined. Divers (n = 7) performed one control BH, and one BH following oral administration of the non-selective cyclooxygenase inhibitor indomethacin (1.2 mg/kg). Arterial blood gases and CBF were measured prior to (baseline), and at BH termination. Compared to control, indomethacin reduced baseline CBF and cerebral delivery of oxygen (CDO

Effect of acetazolamide on cerebral blood flow and capillary patency

1992 ◽  
Vol 73 (5) ◽  
pp. 1756-1761 ◽  
Author(s):  
H. M. Frankel ◽  
E. Garcia ◽  
F. Malik ◽  
J. K. Weiss ◽  
H. R. Weiss
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Gases ◽  
Capillary Perfusion ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Cerebral Capillary ◽  
The Brain

This study investigated the effects 2 h after administration of acetazolamide on cerebral blood flow and the pattern of cerebral capillary perfusion. Arterial blood pressure, heart rate, arterial blood gases, and pH were recorded in two groups of rats along with either regional cerebral blood flow or the percentage of capillary volume per cubic millimeter and number per square millimeter perfused as determined in cortical, thalamic, pontine, and medullary regions of the brain. Blood pressure, heart rate, and arterial PCO2 were not significantly different between the rats receiving acetazolamide (100 mg/kg) and the controls. Arterial blood pH was significantly lower in the acetazolamide rats. Blood flow increased significantly in the cortical (+ 102%), thalamic (+ 89%), and pontine (+ 88%) regions receiving acetazolamide. In control rats, approximately 60% of the capillaries were perfused in all of the examined regions. The percentage of capillaries per square millimeter perfused was significantly greater in the cortical (+ 52%), thalamic (+ 49%), and pontine (+ 47%) regions of acetazolamide rats compared with controls. In the medulla the increases in blood flow and percentage of capillaries perfused were not significant. Thus in the regions that acetazolamide increased cerebral blood flow, it also increased the percentage of capillaries perfused.

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