Influence of Changes in Blood Pressure on Cerebral Perfusion and Oxygenation

Department of Physiology, University of Otago, Dunedin, New Zealand.
Hypertension (Impact Factor: 6.48). 03/2010; 55(3):698-705. DOI: 10.1161/HYPERTENSIONAHA.109.146290
Source: PubMed


Cerebral autoregulation (CA) is a critical process for the maintenance of cerebral blood flow and oxygenation. Assessment of CA is frequently used for experimental research and in the diagnosis, monitoring, or prognosis of cerebrovascular disease; however, despite the extensive use and reference to static CA, a valid quantification of "normal" CA has not been clearly identified. While controlling for the influence of arterial Pco(2), we provide the first clear examination of static CA in healthy humans over a wide range of blood pressure. In 11 healthy humans, beat-to-beat blood pressure (radial arterial), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), end-tidal Pco(2), and cerebral oxygenation (near infrared spectroscopy) were recorded continuously during pharmacological-induced changes in mean blood pressure. In a randomized order, steady-state decreases and increases in mean blood pressure (8 to 14 levels; range: approximately 40 to approximately 125 mm Hg) were achieved using intravenous infusions of sodium nitroprusside or phenylephrine, respectively. MCAv(mean) was altered by 0.82+/-0.35% per millimeter of mercury change in mean blood pressure (R(2)=0.82). Changes in cortical oxygenation index were inversely related to changes in mean blood pressure (slope=-0.18%/mm Hg; R(2)=0.60) and MCAv(mean) (slope=-0.26%/cm . s(-1); R(2)=0.54). There was a progressive increase in MCAv pulsatility with hypotension. These findings indicate that cerebral blood flow closely follows pharmacological-induced changes in blood pressure in otherwise healthy humans. Thus, a finite slope of the plateau region does not necessarily imply a defective CA. Moreover, with progressive hypotension and hypertension there are differential changes in cerebral oxygenation and MCAv(mean).

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Available from: Kate Nicole Thomas, Sep 28, 2014
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    • "Cerebral blood flow is affected by perfusion pressure (Panerai et al. 1999; Dineen et al. 2010; Lucas et al. 2010), metabolism (Iadecola and Nedergaard 2007; Attwell et al. 2011; Paulson et al. 2011) and CO 2 (Ainslie and Burgess 2008; Battisti-Charbonney et al. 2011). The response to CO 2 is thought to be mediated by a direct action of CO 2 on cerebral arteriolar vessels via a change in vessel wall pH to decrease cerebral flow resistance (Lassen 1968; Kontos et al. 1977; Tian et al. 1995). "
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    ABSTRACT: Background and PurposeCerebrovascular reactivity (CVR), measures the ability of the cerebrovasculature to respond to vasoactive stimuli such as CO2. CVR is often expressed as the ratio of cerebral blood flow change to CO2 change. We examine several factors affecting this measurement: blood pressure, stimulus pattern, response analysis and subject position.Methods Step and ramp increases in CO2 were implemented in nine subjects, seated and supine. Middle cerebral artery blood flow velocity (MCAv), and mean arterial pressure (MAP) were determined breath-by-breath. Cerebrovascular conductance (MCAc) was estimated as MCAv/MAP. CVR was calculated from both the relative and absolute measures of MCAc and MCAv responses.ResultsMAP increased with CO2 in some subjects so that relative CVR calculated from conductance responses were less than those calculated from CVR calculated from velocity responses. CVR measured from step responses were affected by the response dynamics, and were less than those calculated from CVR measured from ramp responses. Subject position did not affect CVR.Conclusions(1) MAP increases with CO2 and acts as a confounding factor for CVR measurement; (2) CVR depends on the stimulus pattern used; (3) CVR did not differ from the sitting versus supine in these experiments; (4) CVR calculated from absolute changes of MCAv was less than that calculated from relative changes.
    Brain and Behavior 09/2014; 4(5). DOI:10.1002/brb3.275 · 2.24 Impact Factor
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    • "choroidal vessels in response to relatively long MAP fluctuations (Iester et al., 2007; Okuno et al., 2006). In accordance with previous studies (Lucas et al., 2010; Panerai, 2008), the ratio of the relative change in blood flow to the change in MAP was calculated in this study. This ratio was greater for the RCV than for either the STRA or SNRA after 6 min of exercise in both thermal conditions (see Fig. 3), implying that autoregulation maintained a more stable flow in the retinal circulation than in the choroidal circulation. "
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    ABSTRACT: The hypothesis that heat stress reduces the ocular blood flow response to exhaustive exercise was tested by measuring ocular blood flow, blood pressure, and end-tidal carbon dioxide partial pressure (PETCO2) in 12 healthy males while they performed cycle ergometer exercise at 75% of the maximal heart rate at ambient temperatures of 20°C (control condition) and 35°C (heat condition), until exhaustion. The blood flows in the retinal and choroidal vasculature (RCV), the superior temporal retinal arteriole (STRA) and the superior nasal retinal arteriole (SNRA) were recorded at rest and at 6 and 16 min after the start of exercise period and at exhaustion [after 16 ± 2 min (mean ± SE) and 24 ± 3 min of exercise in the heat and control condition, respectively]. The mean arterial pressure at exhaustion was significantly lower in the heat condition than in the control condition at both 16 min and exhaustion. The degree of PETCO2 reduction did not differ significantly between the two thermal conditions at either 16 min or exhaustion. The blood flow velocity in the RCV significantly increased from the resting baseline value at 6 min in both thermal conditions (32 ± 6% and 25 ± 5% at 20°C and 35°C, respectively). However, at 16 min the increase in RCV blood flow velocity had returned to the resting baseline level only in the heat condition. At exhaustion, the blood flows in the STRA and SNRA had decreased significantly from the resting baseline value in the heat condition (STRA: -19 ± 5% and SNRA: -30 ± 6%), and SNRA blood flow was lower than that in the control condition (-14 ± 6% vs -30 ± 6% at 20°C and 35°C, respectively), despite the finding that both thermal conditions induced the same reductions in PETCO2 and vascular conductance. These findings suggested that the heat condition decreases or suppresses ocular blood flow via attenuation of pressor response during exhaustive exercise.
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    • "Recently the efficacy of both static (Lucas et al. 2010; Perry et al. 2013) and dynamic autoregulation (Edwards et al. 2002; Claassen et al. 2009) has been scrutinized, with evidence for a cerebral circulation being much more pressure passive than originally described (Lassen 1959). Furthermore , there is evidence to indicate that hypercapnia impairs dynamic cerebral autoregulation (Aaslid et al. 1989; Zhang et al. 1998; Ainslie et al. 2005; Maggio et al. 2013). "
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    ABSTRACT: Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure (BP); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ± SD: age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady-state elevations in mean arterial BP (MAP), induced via lower body positive pressure (LBPP). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity (MCAv), BP, partial pressure of end-tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCAv was apparent between eupcapnic baseline and LBPPs (grouped mean 65 ± 11 cm·s−1, all P > 0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P < 0.001 vs. baseline). Conversely, MCAv during the hypercapnic +40 mm Hg stage (Δ31 ± 13 cm·s−1) was greater than hypercapnia alone (Δ25 ± 11 cm·s−1, P = 0.026), due to an increased MAP (Δ14 ± 7 mm Hg, P < 0.001 vs. hypercapnia alone and P = 0.026 vs. hypercapnia +20 mm Hg). As cardiac output and PETCO2 were similar across all hypercapnic stages (all P > 0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation.
    06/2014; 2(6). DOI:10.14814/phy2.12059
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