scholarly journals Autoregulation of cerebral blood flow: influence of the arterial blood pressure on the blood flow through the cerebral cortex.

1966 ◽  
Vol 29 (5) ◽  
pp. 398-403 ◽  
Author(s):  
A M Harper
1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  

Objective To assess the effect of the angiotensin-converting enzyme inhibitor ceronapril on cerebral blood flow (CBF) in patients with moderate hypertension. Design Patients received chlorthalidone 25 mg for 4 weeks, and if diastolic blood pressure remained in the range of 100–115 mm Hg, they were given titrated doses of ceronapril (10–40 mg/d based on blood pressure response) in addition to chlorthalidone for 9 weeks. Setting Outpatient research clinic. Subjects Eligible patients had moderate essential hypertension (diastolic blood pressure 100–115 mm Hg) assessed when the patients were receiving no medications. Thirteen patients were entered into the study; 1 withdrew for reasons unrelated to the study drug. Twelve patients (11 men, 1 woman; mean age 52 y) completed the study. Intervention Ceronapril, given with chlorthalidone. Main Outcome Measures CBF measurements were taken at the start and end of ceronapril therapy using intravenous 133Xe; blood pressures were determined weekly. Results Mean arterial blood pressure decreased from 130 ± 4 to 120 ±7 mm Hg after 4 weeks of chlorthalidone administration, and fell further to 108 ± 8 mm Hg after an additional 9 weeks of combined chlorthalidone-ceronapril therapy (p < 0.05). CBF fell from 44 ± 15 to 34 ± 5 mL/min/100 g during the 9 weeks of combined therapy (p = 0.05). No adverse effects consistent with decreased CBF were observed. The decrease in CBF was not linearly correlated with the change in systemic blood pressure, but was strongly correlated (r = –0.937; p < 0.001) with the initial CBF. Conclusions The decrease in mean arterial blood pressure was not associated with a decrease in CBF. Patients with high CBF may be predisposed to a decrease in CBF when treated with ceronapril and chlorthalidone.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.


2001 ◽  
Vol 280 (5) ◽  
pp. H2162-H2174 ◽  
Author(s):  
Ronney B. Panerai ◽  
Suzanne L. Dawson ◽  
Penelope J. Eames ◽  
John F. Potter

The influence of different types of maneuvers that can induce sudden changes of arterial blood pressure (ABP) on the cerebral blood flow velocity (CBFV) response was studied in 56 normal subjects (mean age 62 yr, range 23–80). ABP was recorded in the finger with a Finapres device, and bilateral recordings of CBFV were performed with Doppler ultrasound of the middle cerebral arteries. Recordings were performed at rest (baseline) and during the thigh cuff test, lower body negative pressure, cold pressor test, hand grip, and Valsalva maneuver. From baseline recordings, positive and negative spontaneous transients were also selected. Stability of Pco 2 was monitored with transcutaneous measurements. Dynamic autoregulatory index (ARI), impulse, and step responses were obtained for 1-min segments of data for the eight conditions by fitting a mathematical model to the ABP-CBFV baseline and transient data (Aaslid's model) and by the Wiener-Laguerre moving-average method. Impulse responses were similar for the right- and left-side recordings, and their temporal pattern was not influenced by type of maneuver. Step responses showed a sudden rise at time 0 and then started to fall back to their original level, indicating an active autoregulation. ARI was also independent of the type of maneuver, giving an overall mean of 4.7 ± 2.9 ( n = 602 recordings). Amplitudes of the impulse and step responses, however, were significantly influenced by type of maneuver and were highly correlated with the resistance-area product before the sudden change in ABP ( r = −0.93, P < 0.0004). These results suggest that amplitude of the CBFV step response is sensitive to the point of operation of the instantaneous ABP-CBFV relationship, which can be shifted by different maneuvers. Various degrees of sympathetic nervous system activation resulting from different ABP-stimulating maneuvers were not reflected by CBFV dynamic autoregulatory responses within the physiological range of ABP.


1981 ◽  
Vol 1 (3) ◽  
pp. 349-356 ◽  
Author(s):  
A. M. Harper ◽  
L. Craigen ◽  
S. Kazda

The effect of the calcium antagonist nimodipine was tested in anaesthetised primates. A rapid intravenous injection of 3 or 10 μg kg−1 produced a transient rise in end-tidal Pco2 and a fall in arterial blood pressure, but 10 min after the injection there was no significant change in CBF. A continuous intravenous infusion of 2 μg kg−1 min−1 caused a modest fall in mean arterial blood pressure and an increase in cerebral blood flow (CBF), which gradually increased to 27% above control after 50 min infusion. There was no significant change in CMRO2. A continuous intracarotid infusion of 0.67 μg kg−1 min−1 caused an increase in CBF of between 46 and 57%. This was further increased to 87% above control after disruption of the blood-brain barrier with hyperosmolar urea. Thirty minutes after the urea, the CBF returned to 43% above control. Twenty minutes after the infusion of nimodipine had been stopped, the CBF had returned to control values. EEG studies in this group showed no obvious increase in electrocortical activity. This evidence suggests that nimodipine has no effect on cerebral metabolism but increases CBF, particularly after disruption of the blood-brain barrier.


1998 ◽  
Vol 275 (1) ◽  
pp. H139-H144 ◽  
Author(s):  
Olivier Régrigny ◽  
Philippe Delagrange ◽  
Elizabeth Scalbert ◽  
Jeffrey Atkinson ◽  
Isabelle Lartaud-Idjouadiene

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.


1973 ◽  
Vol 111 (3) ◽  
pp. 211-217
Author(s):  
KYUHEI IKEDA ◽  
TAKAYUKI IWABUCHI ◽  
TAKASHI KUTSUZAWA ◽  
TAKASHI NAKAMURA

1977 ◽  
Vol 232 (5) ◽  
pp. H495-H499
Author(s):  
M. Manrique ◽  
E. Alborch ◽  
J. M. Delgado

Cerebral blood flow, heart rate, arterial blood pressure, and behavior were studied in conscious goats during electrical stimulation of the diencephalon and mesencephalon. Stimulation of the subthalamic area produced a considerable increase in ipsilateral cerebral blood flow and heart rate, accompanied by either a small or a large increase in systemic arterial blood pressure. Cardiovascular effects were associated with changes in alertness. The increase in cerebral blood flow was partially abolished by previous administration of atropine directly into the internal maxillary artery. Stimulation of the mesencephalic reticular formation caused a marked increase in blood pressure with no change or with some decrease in cerebral blood flow. After administration of phentolamine into the internal maxillary artery, stimulation produced increase in cerebral blood flow. The behavioral response consisted of restlessness and attempted flight. These results suggest the existence of cholinergic vasodilator and adrenergic vasoconstrictor pathways to cerebral blood vessels that may be stimulated electrically.


Sign in / Sign up

Export Citation Format

Share Document