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.

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.

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.

Cortical cerebral blood flow cycling: anesthesia and arterial blood pressure

1995 ◽  
Vol 268 (2) ◽  
pp. H569-H575 ◽  
Author(s):  
S. C. Jones ◽  
J. L. Williams ◽  
M. Shea ◽  
K. A. Easley ◽  
D. Wei
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pressure Change ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Blood Withdrawal ◽  
Cranial Window ◽  
Arterial Blood ◽  
Mean Pressure

Cycling of various cerebral metabolic substances, arterial vascular diameter, and flow has been noted by many workers at a frequency near 0.1 Hz. Suspicion that this phenomenon is dependent on the type of anesthesia led us to investigate the occurrence of cerebral blood flow (CBF) cycling with different anesthetics. Fifteen Sprague-Dawley rats were anesthetized with either pentobarbital (n = 5, 40–50 mg/kg), alpha-chloralose (n = 5, 60 mg/kg), or halothane (n = 5, 1–0.5%). Body temperature was maintained at 37 degrees C. Femoral arterial and venous catheters were placed, and a tracheotomy was performed, permitting artificial ventilation with 30% O2–70% N2. A closed cranial window was formed over a 3-mm diameter craniotomy. Mean arterial pressure (MABP), arterial partial pressures of CO2 and O2 (PaCO2 and PaO2), and pH were controlled and stabilized at normal values. CBF was determined using laser Doppler flowmetry. To induce cycling, MABP was transiently and repeatedly lowered by exsanguination. Fast Fourier analysis of selected 64-s flow recordings (n = 38) was performed. CBF cycling was observed, independent of the type of anesthesia, in all animals. In 36 epochs, cycling was induced when MABP was reduced to a mean pressure of 65 +/- 1.5 mmHg. The mean frequency and amplitude were 0.094 +/- 0.003 Hz and 6.6 +/- 0.5%, respectively. Cycling occurred without blood withdrawal in two epochs. With the use of the blood-withdrawal epochs (n = 36), all three anesthetics shared a common linear slope between amplitude and blood pressure (P < 0.02) and blood pressure change (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Diurnal variation in time to presyncope and associated circulatory changes during a controlled orthostatic challenge

2010 ◽  
Vol 299 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
N. C. S. Lewis ◽  
G. Atkinson ◽  
S. J. E. Lucas ◽  
E. J. M. Grant ◽  
H. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diurnal Variation ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Challenge ◽  
Arterial Blood ◽  
Neurally Mediated Syncope

Epidemiological data indicate that the risk of neurally mediated syncope is substantially higher in the morning. Syncope is precipitated by cerebral hypoperfusion, yet no chronobiological experiment has been undertaken to examine whether the major circulatory factors, which influence perfusion, show diurnal variation during a controlled orthostatic challenge. Therefore, we examined the diurnal variation in orthostatic tolerance and circulatory function measured at baseline and at presyncope. In a repeated-measures experiment, conducted at 0600 and 1600, 17 normotensive volunteers, aged 26 ± 4 yr (mean ± SD), rested supine at baseline and then underwent a 60° head-up tilt with 5-min incremental stages of lower body negative pressure until standardized symptoms of presyncope were apparent. Pretest hydration status was similar at both times of day. Continuous beat-to-beat measurements of cerebral blood flow velocity, blood pressure, heart rate, stroke volume, cardiac output, and end-tidal Pco2 were obtained. At baseline, mean cerebral blood flow velocity was 9 ± 2 cm/s (15%) lower in the morning than the afternoon ( P < 0.0001). The mean time to presyncope was shorter in the morning than in the afternoon (27.2 ± 10.5 min vs. 33.1 ± 7.9 min; 95% CI: 0.4 to 11.4 min, P = 0.01). All measurements made at presyncope did not show diurnal variation ( P > 0.05), but the changes over time (from baseline to presyncope time) in arterial blood pressure, estimated peripheral vascular resistance, and α-index baroreflex sensitivity were greater during the morning tests ( P < 0.05). These data indicate that tolerance to an incremental orthostatic challenge is markedly reduced in the morning due to diurnal variations in the time-based decline in blood pressure and the initial cerebral blood flow velocity “reserve” rather than the circulatory status at eventual presyncope. Such information may be used to help identify individuals who are particularly prone to orthostatic intolerance in the morning.

Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Combined Therapy ◽  
Arterial Blood

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.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

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.

Suctioning and Cerebral Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Base Line ◽  
Arterial Blood

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.

Cerebral blood flow velocity response to induced and spontaneous sudden changes in arterial blood pressure

2001 ◽  
Vol 280 (5) ◽  
pp. H2162-H2174 ◽  
Author(s):  
Ronney B. Panerai ◽  
Suzanne L. Dawson ◽  
Penelope J. Eames ◽  
John F. Potter
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Step Response ◽  
Arterial Blood ◽  
Step Responses

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.

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