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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    • "However, hypertension and dizziness were both highly prevalent and were significantly associated (Lopes et al., 2013). Increased sympathetic influence to the secretion of the norepinephrine , in turn, decreases cerebral oxygenation (Lucas et al., 2010), which might be related with orthostatic intolerance in patients with OHT. OHT should be considered in the differential diagnosis of orthostatic intolerance. "
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    ABSTRACT: Objective: To investigate the frequency and mechanism of orthostatic hypertension (OHT) in patients with orthostatic intolerance. Methods: We retrospectively reviewed 1033 consecutive case series of orthostatic intolerance that underwent autonomic function tests including a head-up tilt test. OHT was defined as a paradoxical orthostatic increase in systolic blood pressure (BP) of at least 20mmHg during the tilt. We collected autonomic parameters during the standardized autonomic function tests, which included the beat-to-beat derived hemodynamic parameters during the tilt table test and compared them with age and sex-matched normal controls and the orthostatic hypotension (OH) group with orthostatic symptoms. Results: We identified 38 (3.7%) patients who showed OHT during the tilt. The increase in mean systolic BP during the tilt was 26.5mmHg. Approximately 87% (33/38) of the OHT patients showed an increase in total peripheral resistance during the tilt. The mean increase in total peripheral resistance from a supine baseline was significantly higher in OHT patients compared to normal controls, but the OH group showed a decrease in mean total peripheral resistance during the tilt. Conclusion: A select few patients with orthostatic dizziness can show OHT during the tilt and they have signs of increased peripheral resistance. Significance: OHT may be considered in the differential diagnosis of orthostatic intolerance.
    Full-text · Article · Jan 2016 · Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology
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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.
    Full-text · Article · Sep 2014 · Brain and Behavior
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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.
    Full-text · Dataset · Jul 2014
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