Role of hypotension in decreasing cerebral blood flow in porcine endotoxemia

1987 ◽  
Vol 253 (4) ◽  
pp. H956-H964 ◽  
Author(s):  
C. F. Miller ◽  
M. J. Breslow ◽  
R. M. Shapiro ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Brain Stem ◽  
Lower Limit ◽  
Cerebral Autoregulation ◽  
Base Line ◽  
Arterial Blood

The role of reduced arterial blood pressure (MAP) in decreasing cerebral blood flow (CBF) during endotoxemia was studied in pentobarbital-anesthetized pigs. Microspheres (15 microns diam) were used to measure regional CBF changes during MAP manipulations in animals with and without endotoxin. Endotoxin (0.2 mg/kg iv) decreased MAP to 50 mmHg and decreased blood flow to the cortex and cerebellum without affecting cerebral cortical oxygen consumption (CMRO2). Elevating MAP from 50 to 70 mmHg during endotoxemia with norepinephrine (1.82 +/- 0.58 micrograms . kg-1 . min-1, iv) did not change cortical blood flow or CMRO2 but increased cerebellar blood flow. Brain stem blood flow was not affected by endotoxin or norepinephrine. When MAP was decreased to 50 mmHg by hemorrhage without endotoxin, no change in blood flow to cortex, cerebellum, or brain stem was observed from base-line levels. These results suggest that decreased MAP below a lower limit for cerebral autoregulation does not account for the decreased CBF observed after endotoxin.

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.

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.

Brain adenosine production in rat during sustained alteration in systemic blood pressure

1980 ◽  
Vol 239 (5) ◽  
pp. H636-H641 ◽  
Author(s):  
H. R. Winn ◽  
J. E. Welsh ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Autoregulation ◽  
Adenine Nucleotides ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Severe Hypotension

Brain production of adenosine and its metabolites, inosine and hypoxanthine was determined in 46 rats during sustained (5 min) reduction in mean arterial blood pressure (MABP) caused by hemorrhage. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), and lactate. Brain tissue was obtained by the freeze-blowing technique. Ventilation was controlled to maintain constant arterial O2 tension, CO2 tension, and pH. When MABP was decreased from 135 + 3 (SE) mmHg to 72 +/- 2 mmHg, within the range of cerebral autoregulation, brain adenosine concentration doubled from 0.55 +/- 0.12 to 1.16 +/- 0.13 nmol/g (P < 0.015). Unlike the changes in adenosine concentrations, adenine nucleotides and PCr remained stable. Lactate varied inversely with MABP. With moderate to severe hypotension (MABP = 45 +/- 3 mmHg), adenosine levels increased almost sixfold. The increment in brain adenosine concentration within the autoregulatory range supports a role for this potent dilator of pial vessels in the regulation of cerebral blood flow.

scholarly journals Dynamic cerebral autoregulation estimates derived from near infrared spectroscopy and transcranial Doppler are similar after correction for transit time and blood flow and blood volume oscillations

2018 ◽  
Vol 40 (1) ◽  
pp. 135-149 ◽  
Author(s):  
Jan Willem J Elting ◽  
Jeanette Tas ◽  
Marcel JH Aries ◽  
Marek Czosnyka ◽  
Natasha M Maurits
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Transit Time ◽  
Phase Difference ◽  
Cerebral Autoregulation ◽  
Cerebral Blood Flow Velocity ◽  
Intraclass Correlation ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

We analysed mean arterial blood pressure, cerebral blood flow velocity, oxygenated haemoglobin and deoxygenated haemoglobin signals to estimate dynamic cerebral autoregulation. We compared macrovascular (mean arterial blood pressure-cerebral blood flow velocity) and microvascular (oxygenated haemoglobin-deoxygenated haemoglobin) dynamic cerebral autoregulation estimates during three different conditions: rest, mild hypocapnia and hypercapnia. Microvascular dynamic cerebral autoregulation estimates were created by introducing the constant time lag plus constant phase shift model, which enables correction for transit time, blood flow and blood volume oscillations (TT-BF/BV correction). After TT-BF/BV correction, a significant agreement between mean arterial blood pressure-cerebral blood flow velocity and oxygenated haemoglobin-deoxygenated haemoglobin phase differences in the low frequency band was found during rest (left: intraclass correlation=0.6, median phase difference 29.5° vs. 30.7°, right: intraclass correlation=0.56, median phase difference 32.6° vs. 39.8°) and mild hypocapnia (left: intraclass correlation=0.73, median phase difference 48.6° vs. 43.3°, right: intraclass correlation=0.70, median phase difference 52.1° vs. 61.8°). During hypercapnia, the mean transit time decreased and blood volume oscillations became much more prominent, except for very low frequencies. The transit time related to blood flow oscillations was remarkably stable during all conditions. We conclude that non-invasive microvascular dynamic cerebral autoregulation estimates are similar to macrovascular dynamic cerebral autoregulation estimates, after TT-BF/BV correction is applied. These findings may increase the feasibility of non-invasive continuous autoregulation monitoring and guided therapy in clinical situations.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

Effect of chronic ANG I-converting enzyme inhibition on aging processes. IV. Cerebral blood flow regulation

1994 ◽  
Vol 267 (3) ◽  
pp. R687-R694 ◽  
Author(s):  
I. Lartaud ◽  
T. Makki ◽  
L. Bray-des-Boscs ◽  
N. Niederhoffer ◽  
J. Atkinson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Cerebrovascular Reactivity ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Age Related

Age-related changes in systemic arterial blood pressure, basal cerebral blood flow (CBF), and CBF regulatory capacity were investigated in awake 6-, 12-, 24-, and 30-mo-old male Wistar (WAG/Rij) rats, one-half of which received the angiotensin I-converting enzyme inhibitor (ACEI) perindopril from 6 mo onward. There was no age-dependent change in mean arterial blood pressure, basal CBF, or cerebrovascular reactivity to hypercapnia, but the lower limit of CBF autoregulation rose from 70 mmHg at 6 and 12 mo to 90 mmHg in 24- and 30-mo-old animals. ACEI lowered mean arterial blood pressure but had no effect on basal CBF or on cerebrovascular reactivity to hypercapnia. ACEI shifted the lower limit of CBF autoregulation to a 20-mmHg-lower level in 12- and 24-mo animals but not in rats treated for 2 yr, i.e., from the ages of 6 to 30 mo. In conclusion, the main age-related change in CBF regulation was an increase in the lower limit of CBF autoregulation to a higher blood pressure level. Treatment with ACEI partially restored the lower limit of CBF autoregulation.

Cerebral autoregulation in migraine with aura: A case control study

Cephalalgia ◽  
2018 ◽  
Vol 39 (5) ◽  
pp. 635-640 ◽  
Author(s):  
Cédric Gollion ◽  
Nathalie Nasr ◽  
Nelly Fabre ◽  
Michèle Barège ◽  
Marc Kermorgant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Transfer Function ◽  
Arterial Blood Pressure ◽  
Migraine With Aura ◽  
Cerebral Autoregulation ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
History Of

Background Migraine with aura is independently associated with increased risk of ischemic stroke, especially in younger subjects. This association might be related to an impairment of cerebral autoregulation, which normally maintains cerebral blood flow independent of arterial blood pressure variations. Methods Patients aged 30–55, fulfilling ICHD-3 beta criteria for migraine with aura, were prospectively enrolled and compared with gender- and age-matched healthy controls without a history of migraine. Patients and controls with a history of stroke or any disease potentially impairing cerebral autoregulation were excluded. We assessed cerebral autoregulation with two different methods: Transfer function analysis, and the correlation coefficient index Mx. The transfer function phase and gain reflect responses of cerebral blood flow velocities to relatively fast fluctuations of arterial blood pressure, whereas Mx also reflects responses to slower arterial blood pressure fluctuations. Results A total of 22 migraine with aura patients (median age [IQR]: 39.5 [12.5] years) and 22 controls (39 [9.75] years) were included. Transfer function parameters and Mx were not different between patients and controls. However, Mx was inversely correlated with age in patients (ρ = −0.567, p = 0.006) and not in controls (ρ = −0.084, p = 0.509). Mx was also inversely correlated with migraine with aura duration (ρ = −0.617, p = 0.002), suggesting improvement of cerebral autoregulation efficiency with disease duration. Conclusions Cerebral autoregulation did not differ between patients and controls aged 30–55. However, cerebral autoregulation efficiency was strongly correlated with migraine with aura duration. Further studies in younger patients are needed to determine whether cerebral autoregulation is impaired early in the course of disease. Trial Registration NCT02708797.

scholarly journals Alternative representation of neural activation in multivariate models of neurovascular coupling in humans

2019 ◽  
Vol 122 (2) ◽  
pp. 833-843 ◽  
Author(s):  
Ronney B. Panerai ◽  
Martha F. Hanby ◽  
Thompson G. Robinson ◽  
Victoria J. Haunton
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Neurovascular Coupling ◽  
Neural Stimulation ◽  
Step Response ◽  
Neural Activation ◽  
Arterial Blood

Neural stimulation leads to increases in cerebral blood flow (CBF), but simultaneous changes in covariates, such as arterial blood pressure (BP) and [Formula: see text], rule out the use of CBF changes as a reliable marker of neurovascular coupling (NVC) integrity. Healthy subjects performed repetitive (1 Hz) passive elbow flexion with their dominant arm for 60 s. CBF velocity (CBFV) was recorded bilaterally in the middle cerebral artery with transcranial Doppler, BP with the Finometer device, and end-tidal CO2 (EtCO2) with capnography. The simultaneous effects of neural stimulation, BP, and [Formula: see text] on CBFV were expressed with a dynamic multivariate model, using BP, EtCO2, and stimulation [ s( t)] as inputs. Two versions of s( t) were considered: a gate function [ sG( t)] or an orthogonal decomposition [ sO( t)] function. A separate CBFV step response was extracted from the model for each of the three inputs, providing estimates of dynamic cerebral autoregulation [CA; autoregulation index (ARI)], CO2 reactivity [vasomotor reactivity step response (VMRSR)], and NVC [stimulus step response (STIMSR)]. In 56 subjects, 224 model implementations produced excellent predictive CBFV correlation (median r = 0.995). Model-generated sO( t), for both dominant (DH) and nondominant (NDH) hemispheres, was highly significant during stimulation (<10−5) and was correlated with the CBFV change ( r = 0.73, P = 0.0001). The sO( t) explained a greater fraction of CBFV variance (~50%) than sG( t) (44%, P = 0.002). Most CBFV step responses to the three inputs were physiologically plausible, with better agreement for the CBFV-BP step response yielding ARI values of 7.3 for both DH and NDH for sG( t), and 6.9 and 7.4 for sO( t), respectively. No differences between DH and NDH were observed for VMRSR or STIMSR. A new procedure is proposed to represent the contribution from other aspects of CBF regulation than BP and CO2 in response to sensorimotor stimulation, as a tool for integrated, noninvasive, assessment of the multiple influences of dynamic CA, CO2 reactivity, and NVC in humans. NEW & NOTEWORTHY A new approach was proposed to identify the separate contributions of stimulation, arterial blood pressure (BP), and arterial CO2 ([Formula: see text]) to the cerebral blood flow (CBF) response observed in neurovascular coupling (NVC) studies in humans. Instead of adopting an empirical gate function to represent the stimulation input, a model-generated function is derived as part of the modeling process, providing a representation of the NVC response, independent of the contributions of BP or [Formula: see text]. This new marker of NVC, together with the model-predicted outputs for the contributions of BP, [Formula: see text] and stimulation, has considerable potential to both quantify and simultaneously integrate the separate mechanisms involved in CBF regulation, namely, cerebral autoregulation, CO2 reactivity and other contributions.

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