Cerebral blood flow response to isocapnic hypoxia during slow-wave sleep and wakefulness

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
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Reactivity ◽  
Slow Wave Sleep ◽  
Transcranial Doppler Ultrasound ◽  
Nrem Sleep ◽  
Left Middle Cerebral Artery ◽  
Arterial Blood ◽  
State Dependent ◽  
Cerebral Vascular

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.

Hypercapnic cerebral vascular reactivity is decreased, in humans, during sleep compared with wakefulness

2003 ◽  
Vol 94 (6) ◽  
pp. 2197-2202 ◽  
Author(s):  
Guy E. Meadows ◽  
Helen M. A. Dunroy ◽  
Mary J. Morrell ◽  
Douglas R. Corfield
Keyword(s):  
Blood Flow ◽  
Vascular Reactivity ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Stage Iii ◽  
Left Middle Cerebral Artery ◽  
Cortical Blood Flow ◽  
Pulsed Doppler Ultrasound ◽  
End Tidal ◽  
Cerebral Vascular

During wakefulness, increases in the partial pressure of arterial CO2 result in marked rises in cortical blood flow. However, during stage III–IV, non-rapid eye movement (NREM) sleep, and despite a relative state of hypercapnia, cortical blood flow is reduced compared with wakefulness. In the present study, we tested the hypothesis that, in normal subjects, hypercapnic cerebral vascular reactivity is decreased during stage III–IV NREM sleep compared with wakefulness. A 2-MHz pulsed Doppler ultrasound system was used to measure the left middle cerebral artery velocity (MCAV; cm/s) in 12 healthy individuals while awake and during stage III–IV NREM sleep. The end-tidal Pco 2(Pet CO2 ) was elevated during the awake and sleep states by regulating the inspired CO2 load. The cerebral vascular reactivity to CO2 was calculated from the relationship between Pet CO2 and MCAV by using linear regression. From wakefulness to sleep, the Pet CO2 increased by 3.4 Torr ( P < 0.001) and the MCAV fell by 11.7% ( P < 0.001). A marked decrease in cerebral vascular reactivity was noted in all subjects, with an average fall of 70.1% ( P = 0.001). This decrease in hypercapnic cerebral vascular reactivity may, at least in part, explain the stage III–IV NREM sleep-related reduction in cortical blood flow.

scholarly journals REGULATION OF CEREBRAL BLOOD FLOW IN HUMANS: PHYSIOLOGY AND CLINICAL IMPLICATIONS OF AUTOREGULATION

2021 ◽  
Author(s):  
Jurgen A.H.R. Claassen ◽  
Dick H.J. Thijssen ◽  
Ronney B Panerai ◽  
Frank M. Faraci
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Function ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Blood Gases ◽  
Clinical Implications ◽  
Arterial Blood ◽  
The Impact

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.

Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

2004 ◽  
Vol 97 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Philip N. Ainslie ◽  
Marc J. Poulin
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Blood Flow Velocity ◽  
Acute Hypoxia ◽  
Random Order ◽  
Transcranial Doppler Ultrasound ◽  
Individual Variability ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
End Tidal

This study examined the effect of high, normal, and uncontrolled end-tidal Pco2 (PetCO2) on the ventilatory, peak cerebral blood flow velocity ( V̄p), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal Po2 was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (PetCO2 +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure V̄p in the middle cerebral artery. The slopes of the linear regressions of ventilation, V̄p, and MAP with arterial O2 saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia ( P < 0.05). Strong, significant correlations were observed between ventilation, V̄p, and MAP with each PetCO2 condition. These data suggest that 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2) in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PetCO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in V̄p and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high V̄p and MAP responses to hypoxia.

scholarly journals Cerebral blood flow regulation in women across menstrual phase: differential contribution of cyclooxygenase to basal, hypoxic, and hypercapnic vascular tone

2016 ◽  
Vol 311 (2) ◽  
pp. R222-R231 ◽  
Author(s):  
Garrett L. Peltonen ◽  
John W. Harrell ◽  
Benjamin P. Aleckson ◽  
Kaylie M. LaPlante ◽  
Meghan K. Crain ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Menstrual Cycle ◽  
Transcranial Doppler Ultrasound ◽  
Follicular Phase ◽  
Cerebrovascular Reactivity ◽  
Menstrual Phase ◽  
Arterial Blood ◽  
End Tidal ◽  
Late Follicular Phase

In healthy young women, basal cerebral blood flow (CBF) and cerebrovascular reactivity may change across the menstrual cycle, but mechanisms remain untested. When compared with the early follicular phase of the menstrual cycle, we hypothesized women in late follicular phase would exhibit: 1) greater basal CBF, 2) greater hypercapnic increases in CBF, 3) greater hypoxic increases in CBF, and 4) increased cyclooxygenase (COX) signaling. We measured middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) in 11 healthy women (23 ± 1 yr) during rest, hypoxia, and hypercapnia. Subjects completed four visits: two during the early follicular (∼ day 3) and two during the late follicular (∼ day 14) phases of the menstrual cycle, with and without COX inhibition (oral indomethacin). Isocapnic hypoxia elicited an SPO2 = 90% and SPO2 = 80% for 5 min each. Separately, hypercapnia increased end-tidal CO2 10 mmHg above baseline. Cerebral vascular conductance index (CVCi = MCAv/MABP·100, where MABP is mean arterial blood pressure) was calculated and a positive change reflected vasodilation (ΔCVCi). Basal CVCi was greater in the late follicular phase ( P < 0.001). Indomethacin decreased basal CVCi (∼37%) and abolished the phase difference ( P < 0.001). Hypoxic ΔCVCi was similar between phases and unaffected by indomethacin. Hypercapnic ΔCVCi was similar between phases, and indomethacin decreased hypercapnic ΔCVCi (∼68%; P < 0.001) similarly between phases. In summary, while neither hypercapnic nor hypoxic vasodilation is altered by menstrual phase, increased basal CBF in the late follicular phase is fully explained by a greater contribution of COX. These data provide new mechanistic insight into anterior CBF regulation across menstrual phases and contribute to our understanding of CBF regulation in women.

Intracarotid Infusion of the Nitric Oxide Synthase Inhibitor, l-NMMA, Modestly Decreases Cerebral Blood Flow in Human Subjects

2000 ◽  
Vol 93 (3) ◽  
pp. 699-707 ◽  
Author(s):  
Shailendra Joshi ◽  
William L. Young ◽  
D. Hoang Duong ◽  
Noeleen D. Ostapkovich ◽  
Beverly D. Aagaard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Reactivity ◽  
Human Subjects ◽  
Nitric Oxide Synthase Inhibitor ◽  
Arginine Infusion ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
Induced Hypertension

Background The authors hypothesized that if nitric oxide (NO) was a determinant of background cerebrovascular tone, intracarotid infusion of NG-monomethyl-L-arginine (L-NMMA), a NO synthase (NOS) inhibitor, would decrease cerebral blood flow (CBF) and intracarotid L-arginine would reverse its effect. Methods In angiographically normal cerebral hemispheres, after the initial dose-escalation studies (protocol 1), the authors determined the effect of intracarotid L-NMMA (50 mg/min for 5 min) on CBF and mean arterial pressure (MAP) over time (protocol 2). Changes in CBF and MAP were then determined at baseline, during L-NMMA infusion, and after L-NMMA during L-arginine infusion (protocol 3). To investigate effects of higher arterial blood concentrations of L-NMMA, changes in CBF and MAP were assessed at baseline and after a bolus dose of L-NMMA (250 mg/1 min), and vascular reactivity was tested by intracarotid verapamil (1 mg/min, protocol 4). CBF changes were also assessed during induced hypertension with intravenous phenylephrine (protocol 5). Results Infusion of L-NMMA (50 mg/min for 5 min, n = 7, protocol 2) increased MAP by 17% (86 +/- 8 to 100 +/- 11 mmHg; P &lt; 0.0001) and decreased CBF by 20% (45 +/- 8 to 36 +/- 6 ml. 100 g-1. min-1; P &lt; 0.005) for 10 min. Intracarotid l-arginine infusion after L-NMMA (protocol 3) reversed the effect of L-NMMA. Bolus L-NMMA (protocol 4) increased MAP by 20% (80 +/- 11 to 96+/-13 mmHg; P&lt; 0.005), but there was no significant decrease in CBF. Intracarotid verapamil increased CBF by 41% (44+/- 8 to 62 +/- 9 ml. 100 g-1. min-1; P&lt; 0.005). Phenylephrine-induced hypertension increased MAP by 20% (79 +/- 9 to 95 +/- 6 mmHg; P = 0.001) but did not affect CBF. Conclusions The results suggest that intracarotid L-NMMA modestly decreases CBF, and the background tone of cerebral resistance vessels may be relatively insensitive to NOS inhibition by the intraarterial route.

scholarly journals Regional Cerebral Blood Flow and Arterial Blood Volume and Their Reactivity to Hypercapnia in Hypertensive and Normotensive Rats

2013 ◽  
Vol 34 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Tae Kim ◽  
J Richard Jennings ◽  
Seong-Gi Kim
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Vascular Reactivity ◽  
Early Stage ◽  
Blood Oxygenation ◽  
Chronic Hypertension ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Arterial Blood Volume

Chronic hypertension induces cerebrovascular remodeling, changing the inner diameter and elasticity of arterial vessels. To examine cerebrovascular morphologic changes and vasodilatory impairment in early-stage hypertension, we measured baseline (normocapnic) cerebral arterial blood volume ( CBVa) and cerebral blood flow ( CBF) as well as hypercapnia-induced dynamic vascular responses in animal models. All experiments were performed with young (3 to 4 month old) spontaneously hypertensive rats (SHR) and control Wistar–Kyoto rats (WKY) under ∼1% isoflurane anesthesia at 9.4 Tesla. Baseline regional CBF values were similar in both animal groups, whereas SHR had significantly lower CBVa values, especially in the hippocampus area. As CBF is maintained by adjusting arterial diameters within the autoregulatory blood pressure range, CBVa is likely more sensitive than CBF for detecting hypertensive-mediated alterations. Unexpectedly, hypercapnia-induced CBF and blood-oxygenation-level-dependent (BOLD) response were significantly higher in SHR as compared with WKY, and the CBF reactivity was highly correlated with the BOLD reactivity in both groups. The higher reactivity in early-stage hypertensive animals indicates no significant vascular remodeling occurred. At later stages of hypertension, the reduced vascular reactivity is expected. Thus, CBF and CBVa mapping may provide novel insights into regional cerebrovascular impairment in hypertension and its progression as hypertension advances.

Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans

2002 ◽  
Vol 80 (8) ◽  
pp. 819-827 ◽  
Author(s):  
Andrea Vovk ◽  
David A Cunningham ◽  
John M Kowalchuk ◽  
Donald H Paterson ◽  
James Duffin
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Blood ◽  
End Tidal

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s–1·mmHg–1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s–1·mmHg–1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min–1·mmHg–1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min–1·mmHg–1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure.

scholarly journals Examination of Potential Mechanisms in the Enhancement of Cerebral Blood Flow by Hypoglycemia and Pharmacological Doses of Deoxyglucose

1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Plasma Lactate ◽  
Insulin Hypoglycemia ◽  
Glucose Levels ◽  
Arterial Blood ◽  
Arterial Plasma

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.

scholarly journals Cerebral blood flow autoregulation in ischemic heart failure

2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Healthy Volunteers ◽  
Neurological Complications ◽  
Ischemic Heart ◽  
Step Response ◽  
Ischemic Heart Failure ◽  
Arterial Blood ◽  
End Tidal

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.

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