MRI study of cerebral blood flow, vascular reactivity, and vascular coupling in systemic hypertension

2021 ◽  
Vol 1753 ◽  
pp. 147224
Author(s):  
Yunxia Li ◽  
Renren Li ◽  
Meng Liu ◽  
Zhiyu Nie ◽  
Eric R. Muir ◽  
...  
2000 ◽  
Vol 98 (1) ◽  
pp. 15-28 ◽  
Author(s):  
Linda Chang ◽  
Charles S. Grob ◽  
Thomas Ernst ◽  
Laurent Itti ◽  
Fred S. Mishkin ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (4) ◽  
pp. e14801 ◽  
Author(s):  
Bálint Várkuti ◽  
Mustafa Cavusoglu ◽  
Alexander Kullik ◽  
Björn Schiffler ◽  
Ralf Veit ◽  
...  

1985 ◽  
Vol 249 (3) ◽  
pp. H672-H680
Author(s):  
P. Lacombe ◽  
M. C. Miller ◽  
J. Seylaz

The cerebral circulatory effects of physiological stimulation of the sympathetic nervous system have been examined in the present study. In lightly anesthetized rabbits, reflex sympathetic activation was provoked by bilateral sinus deafferentation and vagotomy. Regional cerebral blood flow (CBF) was measured by the [14C]-ethanol technique and compared in paired brain structures following unilateral superior cervical ganglionectomy. Two subgroups of hypertensive rabbits were statistically distinguished. In the first (19 of 28 rabbits), CBF in the innervated hemisphere was little modified by hypertension but there was a significant side-to-side difference in CBF between the hemispheres. In the second group (9 rabbits) CBF was markedly increased by the systemic hypertension, and little difference was noted between innervated and denervated hemispheres. We demonstrate that, during acute hypertension, the superior cervical system contributes to cerebrovascular autoregulation; this contribution varies according to the brain region studied. In a subgroup of animals, little sympathetic activity could be evidenced, and it is hypothesized that in these rabbits a vasodilatory system was activated that counteracted the myogenic, autoregulatory responses.


2013 ◽  
Vol 31 (6) ◽  
pp. 990-995 ◽  
Author(s):  
Miho Ota ◽  
Noriko Sato ◽  
Yasuhiro Nakata ◽  
Kimiteru Ito ◽  
Kouhei Kamiya ◽  
...  

Author(s):  
Jurgen A.H.R. Claassen ◽  
Dick H.J. Thijssen ◽  
Ronney B Panerai ◽  
Frank M. Faraci

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.


2004 ◽  
Vol 97 (4) ◽  
pp. 1343-1348 ◽  
Author(s):  
Guy E. Meadows ◽  
Denise M. O'Driscoll ◽  
Anita K. Simonds ◽  
Mary J. Morrell ◽  
Douglas R. Corfield

Nocturnal hypoxia is a major pathological factor associated with cardiorespiratory disease. During wakefulness, a decrease in arterial O2 tension results in a decrease in cerebral vascular tone and a consequent increase in cerebral blood flow; however, the cerebral vascular response to hypoxia during sleep is unknown. In the present study, we determined the cerebral vascular reactivity to isocapnic hypoxia during wakefulness and during stage 3/4 non-rapid eye movement (NREM) sleep. In 13 healthy individuals, left middle cerebral artery velocity (MCAV) was measured with the use of transcranial Doppler ultrasound as an index of cerebral blood flow. During wakefulness, in response to isocapnic hypoxia (arterial O2 saturation −10%), the mean (±SE) MCAV increased by 12.9 ± 2.2% ( P < 0.001); during NREM sleep, isocapnic hypoxia was associated with a −7.4 ± 1.6% reduction in MCAV ( P < 0.001). Mean arterial blood pressure was unaffected by isocapnic hypoxia ( P > 0.05); R-R interval decreased similarly in response to isocapnic hypoxia during wakefulness (−21.9 ± 10.4%; P < 0.001) and sleep (−20.5 ± 8.5%; P < 0.001). The failure of the cerebral vasculature to react to hypoxia during sleep suggests a major state-dependent vulnerability associated with the control of the cerebral circulation and may contribute to the pathophysiologies of stroke and sleep apnea.


2007 ◽  
Vol 34 (5) ◽  
pp. 322-329 ◽  
Author(s):  
S. Guyer ◽  
M. Kosel ◽  
S. Altrichter ◽  
M. El-Koussy ◽  
R. Haemmig ◽  
...  

2012 ◽  
Vol 8 (4S_Part_9) ◽  
pp. P350-P350
Author(s):  
Xiaowei Song ◽  
Chen Wei ◽  
Ryan D'Arcy ◽  
Steven Beyea ◽  
Careesa Liu ◽  
...  

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