An Anatomical Model of the Cerebral Vasculature and the Autoregulation of Cerebral Blood Flow

Author(s):  
C. Lucas ◽  
S. J. Payne
1964 ◽  
Vol 206 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Martin Reivich

The effect of arterial Pco2 in the control of cerebral hemodynamics over the full range of responsiveness of the cerebral vasculature was studied in the rhesus monkey. Cerebral perfusion pressure and arterial O2 saturation were controlled so that they produced no significant effect on the cerebral circulation. Other possible sources of error, e.g., blood temperature, effect of anesthesia, development of metabolic acidosis, and validity of internal jugular measurements of cerebral blood flow were evaluated. Arterial Pco2 was varied from 5 to 418 mm Hg in eight animals. The minimum and maximum cerebral blood flows obtained were 18 and 140 ml/min 100 g, respectively. These values were approached when the arterial Pco2 was in the range of 10–15 mm Hg and 150 mm Hg, respectively. At these levels of arterial Pco2 the maximum and minimum cerebrovascular resistance occurred. These values were 4.78 and 0.63 mm Hg/ml/min per 100 g, respectively. A mathematical analysis of the data enabled equations relating arterial Pco2 to cerebrovascular resistance and to cerebral blood flow to be derived. Values predicted by these equations compare favorably with the actual measured data and with similar data in the literature.


2015 ◽  
Vol 308 (5) ◽  
pp. R379-R390 ◽  
Author(s):  
Fan Fan ◽  
Aron M. Geurts ◽  
Sydney R. Murphy ◽  
Mallikarjuna R. Pabbidi ◽  
Howard J. Jacob ◽  
...  

We have reported that a reduction in renal production of 20-HETE contributes to development of hypertension in Dahl salt-sensitive (SS) rats. The present study examined whether 20-HETE production is also reduced in the cerebral vasculature of SS rats and whether this impairs the myogenic response and autoregulation of cerebral blood flow (CBF). The production of 20-HETE, the myogenic response of middle cerebral arteries (MCA), and autoregulation of CBF were compared in SS, SS-5BN rats and a newly generated CYP4A1 transgenic rat. 20-HETE production was 6-fold higher in cerebral arteries of CYP4A1 and SS-5BN than in SS rats. The diameter of the MCA decreased to 70 ± 3% to 65 ± 6% in CYP4A1 and SS-5BN rats when pressure was increased from 40 to 140 mmHg. In contrast, the myogenic response of MCA isolated from SS rats did not constrict. Administration of a 20-HETE synthesis inhibitor, HET0016, abolished the myogenic response of MCA in CYP4A1 and SS-5BN rats but had no effect in SS rats. Autoregulation of CBF was impaired in SS rats compared with CYP4A1 and SS-5BN rats. Blood-brain barrier leakage was 5-fold higher in the brain of SS rats than in SS-5BN and SS.CYP4A1 rats. These findings indicate that a genetic deficiency in the formation of 20-HETE contributes to an impaired myogenic response in MCA and autoregulation of CBF in SS rats and this may contribute to vascular remodeling and cerebral injury following the onset of hypertension.


2019 ◽  
Vol 127 (5) ◽  
pp. 1197-1205 ◽  
Author(s):  
Shigehiko Ogoh

This review summarizes the interaction between the regulatory system of respiration and cerebral vasculature. Some clinical reports provide evidence for the association between these two physiological regulatory systems. Physiologically, arterial carbon dioxide concentration is mainly regulated by two feedback control systems: respiration and cerebral blood flow. In other words, both of these systems are sensitive to the same mediator, i.e., carbon dioxide, at a set point. In addition, respiratory dysfunction alters various physiological factors that affect the cerebral vasculature. Therefore, it is physiologically plausible that these systems are closely linked. The regulation of arterial carbon dioxide concentration affected by respiration and cerebral blood flow may be a key factor for a rise in the risk of brain disease in the patients with respiratory dysfunction. For example, the management of respiratory disease (e.g., patients with chronic obstructive pulmonary disease) and the use of prophylactic therapy are essential to reduce the risk of stroke.


2017 ◽  
Vol 27 (8) ◽  
pp. 1606-1613 ◽  
Author(s):  
Rachel Wong ◽  
Waheed Ahmad ◽  
Allan Davies ◽  
Neil Spratt ◽  
Andrew Boyle ◽  
...  

AbstractBackgroundSurvival into adult life in patients with aortic coarctation is typical following surgical and catheter-based techniques to relieve obstruction. Late sequelae are recognised, including stroke, hypertension, and intracerebral aneurysm formation, with the underlying mechanisms being unclear. We hypothesised that patients with a history of aortic coarctation may have abnormalities of cerebral blood flow compared with controls.MethodsPatients with a history of aortic coarctation underwent assessment of cerebral vascular function. Vascular responsiveness of intracranial vessels to hypercapnia and degree of cerebral artery stiffness using Doppler-derived pulsatility indices were used. Response to photic stimuli was used to assess neurovascular coupling, which reflects endothelial function in response to neuronal activation. Patient results were compared with age- and sex-matched controls.ResultsA total of 13 adult patients (males=10; 77%) along with 13 controls underwent evaluation. The mean age was 36.1±3.7 years in the patient group. Patients with a background of aortic coarctation were noted to have increased pulse pressure on blood pressure assessment at baseline with increased intracranial artery stiffness compared with controls. Patients with a history of aortic coarctation had less reactive cerebral vasculature to hypercapnic stimuli and impaired neurovascular coupling compared with controls.ResultsAdult patients with aortic coarctation had increased intracranial artery stiffness compared with controls, in addition to cerebral vasculature showing less responsiveness to hypercapnic and photic stimuli. Further studies are required to assess the aetiology and consequences of these documented abnormalities in cerebral blood flow in terms of stroke risk, cerebral aneurysm formation, and cognitive dysfunction.


2001 ◽  
Vol 120 (5) ◽  
pp. A637-A637
Author(s):  
Y RINGEL ◽  
D DROSSMAN ◽  
T TURKINGTON ◽  
B BRADSHAW ◽  
R COLEMAN ◽  
...  

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