Philip N Ainslie

University of British Columbia - Okanagan, Kelowna, British Columbia, Canada

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Publications (180)568.07 Total impact

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    ABSTRACT: Transfer function analysis (TFA) is a frequently used method to assess dynamic cerebral autoregulation (CA) using spontaneous oscillations in blood pressure (BP) and cerebral blood flow velocity (CBFV). However, controversies and variations exist in how research groups utilise TFA, causing high variability in interpretation. The objective of this study was to evaluate between-centre variability in TFA outcome metrics. 15 centres analysed the same 70 BP and CBFV datasets from healthy subjects (n = 50 rest; n = 20 during hypercapnia); 10 additional datasets were computer-generated. Each centre used their in-house TFA methods; however, certain parameters were specified to reduce a priori between-centre variability. Hypercapnia was used to assess discriminatory performance and synthetic data to evaluate effects of parameter settings. Results were analysed using the Mann-Whitney test and logistic regression. A large non-homogeneous variation was found in TFA outcome metrics between the centres. Logistic regression demonstrated that 11 centres were able to distinguish between normal and impaired CA with an AUC>0.85. Further analysis identified TFA settings that are associated with large variation in outcome measures. These results indicate the need for standardisation of TFA settings in order to reduce between-centre variability and to allow accurate comparison between studies. Suggestions on optimal signal processing methods are proposed.
    Medical Engineering & Physics 01/2015; in press:2014. · 1.78 Impact Factor
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    ABSTRACT: The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers (n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing ('clamp') was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23 to 37 mm Hg (30±7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54±24% versus 34±26%, respectively; however, CBF increased similarly between apnea and clamp (93.6±28% and 83.4±38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.Journal of Cerebral Blood Flow & Metabolism advance online publication, 5 November 2014; doi:10.1038/jcbfm.2014.170.
    11/2014;
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    ABSTRACT: Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250 mg, three times-a-day for 48 h) to prevent increases in PASP, and (3) isocapnic hypoxia with AZ and 8.4% NaHCO3 infusion (AZ+HCO3−) to control for AZ-induced acidosis. Isocapnic hypoxia (20 min) was maintained by end-tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic-hypoxia condition to determine pH, [HCO3−], and PaCO2. AZ decreased pH (-0.08 ± 0.01), [HCO3−] (-7.1 ± 0.7 mmol/l), and PaCO2 (-4.5 ± 1.4 mmHg; p<0.01), while intravenous NaHCO3 restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (p<0.05), a main effect of condition expressed an 11 ± 2% reduction in PASP from control (p<0.001) following AZ administration while intravenous NaHCO3 partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (p<0.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H+ concentration or PaCO2.This article is protected by copyright. All rights reserved
    The Journal of Physiology 11/2014; · 4.38 Impact Factor
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    ABSTRACT: Heart transplant recipients are at an increased risk for cerebral hemorrhage and ischemic stroke; yet, the exact mechanism for this derangement remains unclear. We hypothesized that alterations in cerebrovascular regulation is principally involved. To test this hypothesis, we studied cerebral pressure-flow dynamics in 8 clinically stable male heart transplant recipients (62±8 years of age and 9±7 years post transplant, mean±SD), 9 male age-matched controls (63±8 years), and 10 male donor controls (27±5 years). To increase blood pressure variability and improve assessment of the pressure-flow dynamics, subjects performed squat-stand maneuvers at 0.05 and 0.10 Hz. Beat-to-beat blood pressure, middle cerebral artery velocity, and end-tidal carbon dioxide were continuously measured during 5 minutes of seated rest and throughout the squat-stand maneuvers. Cardiac baroreceptor sensitivity gain and cerebral pressure-flow responses were assessed with linear transfer function analysis. Heart transplant recipients had reductions in R-R interval power and baroreceptor sensitivity low frequency gain (P<0.01) compared with both control groups; however, these changes were unrelated to transfer function metrics. Thus, in contrast to our hypothesis, the increased risk of cerebrovascular complication after heart transplantation does not seem to be related to alterations in cerebral pressure-flow dynamics. Future research is, therefore, warranted.
    Hypertension 10/2014; · 6.87 Impact Factor
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    ABSTRACT: The incidence of vasovagal syncope is more common in the morning. Previous researchers have reported negligible diurnal variation in the physiological responses associated with initial orthostatic hypotension (IOH). Nevertheless, physical activity and sleep prior to morning and afternoon test times have not been controlled and may influence the findings. We designed a semi-constant routine protocol to examine diurnal variation in cardiorespiratory and cerebrovascular responses to active standing.
    European journal of applied physiology. 10/2014;
  • Mike Stembridge, Philip N. Ainslie, Rob Shave
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    ABSTRACT: Both short-term and life-long high altitude (HA) exposure challenge the cardiovascular system to meet the metabolic demand for oxygen (O2) in a hypoxic environment. As the demand for O2 delivery increases during exercise, the circulatory component of oxygen transport is placed under additional stress. Acute adaptation and chronic remodelling of cardiac structure and function may occur to facilitate O2 delivery in lowlanders during sojourn to high altitude and in permanent highland residents. However our understanding of cardiac structural and functional adaption in Sherpa remains confined to a higher maximal heart rate, lower pulmonary vascular resistance and no differences in resting cardiac output. Ventricular form and function are intrinsically linked through the left ventricular (LV) mechanics that facilitate efficient ejection, minimise myofibre stress during contraction and aid diastolic recoil. Recent examination of LV mechanics has allowed detailed insight into fundamental cardiac adaptation in HA Sherpa. In this symposium report, we review recent advances in our understanding of LV function in both lowlanders and Sherpa at rest, and discuss the potential consequences for exercise capacity. Collectively, data indicate chronic structural ventricular adaptation, with adult Sherpa having smaller absolute and relative LV size. Consistent with structural remodelling, cardiac mechanics also differ in Sherpa when compared to lowlanders at HA. These differences are characterised by a reduction in resting systolic deformation and slower diastolic untwisting, a surrogate of relaxation. These changes may reflect a functional cardiac adaptation that affords Sherpa the same mechanical reserve seen in lowlanders at sea level, which is absent when they ascend to HA.This article is protected by copyright. All rights reserved
    Experimental physiology 10/2014; · 3.17 Impact Factor
  • Philip N Ainslie, Ryan L Hoiland
    Journal of applied physiology (Bethesda, Md. : 1985). 09/2014;
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    ABSTRACT: We examined two novel hypotheses: 1) That orthostatic tolerance (OT) would be prolonged when hyperventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and 2) that pharmacological reductions in cerebral blood flow (CBF) at baseline would lower the “CBF reserve”, and ultimately reduce OT. In Study 1 (n = 24; aged 25±4 y) participants underwent progressive lower-body negative pressure (LBNP) until pre-syncope; end-tidal carbon dioxide (PETCO2) was clamped at baseline levels (isocapnic trial) or uncontrolled. In Study 2 (n = 10; aged 25±4 y), CBF was pharmacologically reduced by administration of indomethacin (INDO; 1.2 mg/kg) or unaltered (placebo) followed by LBNP to pre-syncope. Beat-by-beat measurements of middle cerebral artery blood flow velocity (MCAv; transcranial Doppler), heart rate (ECG), blood pressure (BP; Finometer) and end-tidal gases were obtained continuously. In a subset of subjects’ arterial-to-jugular venous differences were obtained to examine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxygen delivery and extraction. Study 1: During the isocapnic trial, PETCO2 was successfully clamped at baseline levels at pre-syncope (38.3±2.7 vs. 38.5±2.5 mm Hg respectively; P = 0.50). In the uncontrolled trial, PETCO2 at pre-syncope was reduced by 10.9±3.9 mm Hg (P≤0.001). Compared to the isocapnic trial, the decline in mean MCAv was 15±4 cm∙s−1 (35%; P≤0.001) greater in the uncontrolled trial, yet the time to pre-syncope was comparable between trials (544±130 v 572±180 s; P = 0.30). Study 2: Compared to placebo, INDO reduced resting MCAv by 19±4 cm∙s−1 (31%; P≤0.001), but time to pre-syncope remained similar between trials (placebo: 1123±138 vs. INDO: 1175±212 s; P = 0.53). The brain extracted more oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for reductions in delivery. In summary, cerebral hypoperfusion either at rest or induced by hypocapnia at pre-syncope does not impact OT, likely due to a compensatory increase in oxygen extraction.This article is protected by copyright. All rights reserved
    The Journal of Physiology 09/2014; · 4.38 Impact Factor
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    ABSTRACT: Cerebral blood flow responses to transient blood pressure challenges are frequently attributed to cerebral autoregulation (CA) yet accumulating evidence indicates vascular properties like compliance are also influential. We hypothesized that middle cerebral blood velocity (MCAv) dynamics during or following a transient blood pressure perturbation can be accurately explained by the Windkessel mechanism. Eighteen volunteers underwent blood pressure manipulations including bilateral thigh cuff deflation (TC) and sit-to-stand (STS) maneuvers under normocapnic and hypercapnic (5% CO2) conditions. Pressure-flow recordings were analyzed using a Windkessel analysis approach that partitions the frequency-dependent resistance and compliance contributions to MCAv dynamics. The Windkessel was typically able to explain more than 50% of the MCAv variance as indicated by R2 values for both the flow recovery and post recovery phase. The most consistent predictors of MCAv dynamics under the control condition were the Windkessel capacitive gain and high frequency resistive gain. However, there were significant inter-individual variations in the composition of Windkessel predictors. Hypercapnia consistently reduced the capacitive gain and enhanced the low frequency (0.04-0.20 Hz) resistive gain for both TC and STS trials. These findings indicate that: 1) MCAv dynamics during acute transient hypotension challenges are dominated by cerebrovascular Windkessel properties independent of CA; 2) there is significant heterogeneity in Windkessel properties between individuals; and 3) hemodynamic effects of hypercapnia during transient blood pressure challenges primarily reflect changes in Windkessel properties rather than pure CA impairment.
    Journal of applied physiology (Bethesda, Md. : 1985). 08/2014;
  • Anthony R. Bain, Philip N. Ainslie
    The Journal of Physiology 07/2014; 592(14). · 4.38 Impact Factor
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    Philip N Ainslie, Andrew W Subudhi
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    ABSTRACT: Abstract Ainslie, Philip N., and Andrew W. Subudhi. Invited Review: Cerebral blood flow at high altitude. High Alt Med Biol. 15:133-140, 2014.-This brief review traces the last 50 years of research related to cerebral blood flow (CBF) in humans exposed to high altitude. The increase in CBF within the first 12 hours at high altitude and its return to near sea level values after 3-5 days of acclimatization was first documented with use of the Kety-Schmidt technique in 1964. The degree of change in CBF at high altitude is influenced by many variables, including arterial oxygen and carbon dioxide tensions, oxygen content, cerebral spinal fluid pH, and hematocrit, but can be collectively summarized in terms of the relative strengths of four key integrated reflexes: 1) hypoxic cerebral vasodilatation; 2) hypocapnic cerebral vasoconstriction; 3) hypoxic ventilatory response; and 4) hypercapnic ventilatory response. Understanding the mechanisms underlying these reflexes and their interactions with one another is critical to advance our understanding of global and regional CBF regulation. Whether high altitude populations exhibit cerebrovascular adaptations to chronic levels of hypoxia or if changes in CBF are related to the development of acute mountain sickness are currently unknown; yet overall, the integrated CBF response to high altitude appears to be sufficient to meet the brain's large and consistent demand for oxygen. This short review is organized as follows: An historical overview of the earliest CBF measurements collected at high altitude introduces a summary of reported CBF changes at altitude over the last 50 years in both lowlanders and high-altitude natives. The most tenable candidate mechanism(s) regulating CBF at altitude are summarized with a focus on available data in humans, and a role for these mechanisms in the pathophysiology of AMS is considered. Finally, suggestions for future directions are provided.
    High altitude medicine & biology. 06/2014; 15(2):133-40.
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    ABSTRACT: Short-term high altitude (HA) exposure raises pulmonary artery systolic pressure (PASP) and decreases left ventricular (LV) volumes. However, relatively little is known of the long-term cardiac consequences of prolonged exposure in Sherpa, a highly-adapted HA population. To investigate short-term adaptation and potential long-term cardiac remodelling, we studied ventricular structure and function in Sherpa at 5050 m (n=11; 31±13 y, mass 68±10 kg, height 169±6 cm) and lowlanders at sea level (SL) and following 10±3 d at 5050 m (n=9; 34±7 y, mass 82±10 kg, height 177±6 cm) using conventional and speckle-tracking echocardiography. At HA, PASP was higher in Sherpa and lowlanders when compared to lowlanders at SL (both P<0.05). Sherpa had smaller right ventricular (RV) and LV stroke volumes than lowlanders at SL with lower RV systolic strain (P<0.05) but similar LV systolic mechanics. In contrast to LV systolic mechanics, LV diastolic untwisting velocity was significantly lower in Sherpa when compared to lowlanders at both SL and HA. After partial acclimatization, lowlanders demonstrated no change in RV end-diastolic area, however both RV strain and LV end-diastolic volume were reduced. In conclusion, short-term hypoxia induced a reduction in RV systolic function that was also evident in Sherpa following chronic exposure. We propose this was consequent to a persistently higher PASP. In contrast to the RV, remodelling of LV volumes and normalization of systolic mechanics indicate structural and functional adaptation to HA. However, altered LV diastolic relaxation after chronic hypoxic exposure may reflect differential remodelling of systolic and diastolic LV function.
    Journal of applied physiology (Bethesda, Md. : 1985). 05/2014;
  • Source
    Philip N. Ainslie
    Experimental physiology 05/2014; 99(5). · 3.17 Impact Factor
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    ABSTRACT: We examined the hypothesis that changes in the cerebrovascular resistance index (CVRi), independent of blood pressure (BP), will influence the dynamic relationship between blood pressure and cerebral blood flow in humans. We altered CVRi with (via controlled hyperventilation) and without (via Indomethacin (INDO; 1.2 mg/kg) changes in PaCO2. Sixteen subjects (12 male, 27±7yrs) were tested on two occasions (INDO and hypocapnia) separated by >48hr. Each test incorporated seated rest (5-min), followed by squat-stand maneuvers to increase BP variability and improve assessment of the pressure-flow dynamics using linear transfer function analysis (TFA). Beat-to-beat BP, middle cerebral artery (MCAv), posterior cerebral artery (PCAv) velocity and end-tidal PCO2 were monitored. Dynamic pressure-flow relations were quantified using TFA between BP and MCAv/PCAv in the very low and low frequencies through the driven squat-stand maneuvers at 0.05 and 0.10 Hz. MCAv and PCAv reductions by INDO and hypocapnia were well-matched and CVRi was comparably elevated (P<0.001). During the squat-stand maneuvers (0.05 and 0.10 Hz), the point estimates of absolute gain were universally reduced and phase was increased under both conditions. In addition to an absence of regional differences, our findings indicate that alterations in CVRi independent of PaCO2 can alter cerebral pressure-flow dynamics. These findings are consistent with the concept of CVRi being a key factor that should be considered in the correct interpretation of cerebral pressure-flow dynamics as indexed using TFA metrics.
    Journal of Applied Physiology 04/2014; · 3.48 Impact Factor
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    ABSTRACT: Transfer function analysis (TFA) is a frequently used method to assess dynamic cerebral autoregulation (CA) using spontaneous oscillations in blood pressure (BP) and cerebral blood flow velocity (CBFV). However, controversies and variations exist in how research groups utilise TFA, causing high variability in interpretation. The objective of this study was to evaluate between-centre variability in TFA outcome metrics. 15 centres analysed the same 70 BP and CBFV datasets from healthy subjects (n=50 rest; n=20 during hypercapnia); 10 additional datasets were computer-generated. Each centre used their in-house TFA methods; however, certain parameters were specified to reduce a priori between-centre variability. Hypercapnia was used to assess discriminatory performance and synthetic data to evaluate effects of parameter settings. Results were analysed using the Mann-Whitney test and logistic regression. A large non-homogeneous variation was found in TFA outcome metrics between the centres. Logistic regression demonstrated that 11 centres were able to distinguish between normal and impaired CA with an AUC>0.85. Further analysis identified TFA settings that are associated with large variation in outcome measures. These results indicate the need for standardisation of TFA settings in order to reduce between-centre variability and to allow accurate comparison between studies. Suggestions on optimal signal processing methods are proposed.
    Medical Engineering & Physics 04/2014; · 1.78 Impact Factor
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    ABSTRACT: The arterial baroreflex is critical to both short and long-term regulation of blood pressure. However, human baroreflex research has been largely limited to the association between blood pressure and cardiac period (or heart rate) or indices of vascular sympathetic function. Over the past decade, emerging techniques based on carotid ultrasound imaging have allowed new means of understanding and measuring the baroreflex. In this review, we describe the assessment of the mechanical and neural components of the baroreflex through the use of carotid ultrasound imaging. The mechanical component refers to the change in carotid artery diameter in response to changes in arterial pressure, and the neural component refers to the change in R-R interval (cardiac baroreflex) or muscle sympathetic nerve activity (sympathetic baroreflex) in response to this barosensory vessel stretch. The key analytical concepts and techniques are discussed, with a focus on the assessment of baroreflex sensitivity via the modified Oxford method. We illustrate how the application of carotid ultrasound imaging has contributed to a greater understanding of baroreflex physiology in humans, covering topics such as ageing and diurnal variation, and physiological challenges including exercise, postural changes and mental stress.This article is protected by copyright. All rights reserved.
    Acta Physiologica 04/2014; · 4.38 Impact Factor
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    ABSTRACT: We examined whether: 1) global-cerebral blood flow (CBF) would increase across a six hours bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in vertebral artery (VA) than in the internal carotid artery (ICA) 2); additional increases in global-CBF will be evident following an alpha (α)1-adrenergic blockade, via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA- and VA-flow were obtained in normoxia (baseline) and following 60, 210 and 330 min of hypoxia (FIO2=0.11). Ninety minutes prior to final assessment, participants received a α1-adrenoreceptor blocker (Prazosin: 1 mg/20 kg body mass) or placebo. Compared to baseline, following 60, 220 and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow)*2] increased by 160 ± 52 ml/min (+28%; P=0.05), 134 ± 23 ml/min (+23%; P=0.02), 113 ± 51 (+19%; P=0.27), respectively. Compared to baseline, ICAFlow increased by 23% following 60 min of hypoxia (P=0.06), after which it progressively declined. The percentage increase in VA-flow was consistently larger than ICA-flow during hypoxia by ~20% (P=0.002). Compared to baseline, ICA and VA diameters increased during hypoxia by ~9% and ~12%, respectively (P≤0.05), and were correlated to the reductions in SaO2. Flow and diameters were unaltered following α1-blockade (P≥0.10). In conclusion, elevations in global-CBF during acute hypoxia are partly mediated via greater increases in VA-flow compared to ICA-flow; this regional difference was unaltered following α1-blockade, indicating that a heightened SNA with hypoxia does not constrain further dilation of larger extracrainal blood vessels.
    Journal of Applied Physiology 03/2014; · 3.48 Impact Factor
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    ABSTRACT: Episodic increases in cerebrovascular perfusion and shear stress may have beneficial impacts on endothelial function that improve brain health. We hypothesised that water immersion to the level of the right atrium in humans would increase cerebral perfusion. We continuously measured, in 9 young (mean±SD, 24.6 ± 2.0 yrs) healthy men, systemic hemodynamic variables along with blood flows in the common carotid and middle and posterior cerebral arteries during controlled filling and emptying of a water tank to the level of the right atrium. Mean arterial pressure (80 ± 9 vs 91 ± 12 mmHg, P<0.05), cardiac output (4.8 ± 0.7 vs 5.1±0.6 L/min, P<0.05) and end-tidal carbon dioxide (PetCO2, 39.5 ± 2.0 vs 44.4 ± 3.5 mmHg, P<0.05) increased with water immersion, along with middle (59 ± 6 vs 64 ± 6 cm/s, P<0.05) and posterior cerebral artery blood flow velocities (41 ± 9 vs 44 ± 10 cm/s, P<0.05). These changes were reversed when the tank was emptied. Water immersion is associated with haemodynamic and PetCO2 changes, which increase cerebral blood velocities in humans. This study provides an evidence base for future studies to examine the potential addictive effect of exercise in water on improving cerebrovascular health.
    AJP Regulatory Integrative and Comparative Physiology 02/2014; · 3.28 Impact Factor
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    ABSTRACT: Individuals with high-level spinal cord injury (SCI) experience low blood pressure (BP) and cognitive impairments. Such dysfunction may be mediated in part by impaired neurovascular coupling (NVC) (i.e., cerebral blood flow responses to neurologic demand). Ten individuals with SCI >T6 spinal segment, and 10 age- and sex-matched controls were assessed for beat-by-beat BP, as well as middle and posterior cerebral artery blood flow velocity (MCAv, PCAv) in response to a NVC test. Tests were repeated in SCI after 10 mg midodrine (alpha1-agonist). Verbal fluency was measured before and after midodrine in SCI, and in the control group as an index of cognitive function. At rest, mean BP was lower in SCI (70±10 versus 92±14 mm Hg; P<0.05); however, PCAv conductance was higher (0.56±0.13 versus 0.39±0.15 cm/second/mm Hg; P<0.05). Controls exhibited a 20% increase in PCAv during cognition; however, the response in SCI was completely absent (P<0.01). When BP was increased with midodrine, NVC was improved 70% in SCI, which was reflected by a 13% improved cognitive function (P<0.05). Improvements in BP were related to improved cognitive function in those with SCI (r(2)=0.52; P<0.05). Impaired NVC, secondary to low BP, may partially mediate reduced cognitive function in individuals with high-level SCI.Journal of Cerebral Blood Flow & Metabolism advance online publication, 29 January 2014; doi:10.1038/jcbfm.2014.3.
    Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 01/2014; · 5.46 Impact Factor
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    ABSTRACT: Individuals with spinal cord injury (SCI) above the T6 spinal segment suffer from orthostatic intolerance. How cerebral blood flow (CBF) responds to orthostatic challenges in SCI is poorly understood. Furthermore, it is unclear how interventions meant to improve orthostatic tolerance in SCI influence CBF. This study aimed to examine: 1) the acute regional CBF responses to rapid changes in blood pressure (BP) during orthostatic stress in those with SCI and able-bodied individuals 2) the effect of Midodrine (alpha1-agonist) on orthostatic tolerance and CBF regulation in SCI. Ten individuals with SCI >T6, and 10 age-and sex-matched controls (AB) had beat-by-beat BP, as well as middle and posterior cerebral artery blood velocity (MCAv, PCAv) recorded during a progressive tilt-test to quantify the acute CBF response, and orthostatic tolerance. Dynamic MCAv and PCAv to BP relationships were evaluated continuously in the time domain and frequency domain (via transfer function analysis). The SCI group was tested again after administration of 10 mg Midodrine to elevate BP. Coherence (i.e., linearity) was elevated in SCI between BP-MCAv and BP-PCAv by 35% and 22% respectively compared to AB, while SCI BP-PCAv gain (i.e., magnitudinal relationship) was reduced 30% compared to AB (all P<0.05). The acute (i.e., 0-30s after tilt) MCAv and PCAv responses were similar between groups. In SCI, Midodrine led to improved PCAv responses 30-60s following tilt (10±3 vs. 4±2 %decline;P<0.05), and a 59% improvement in orthostatic tolerance (P<0.01). The vertebrobasilar region may be particularly susceptible to hypoperfusion in SCI, leading to increased orthostatic intolerance.
    Journal of Applied Physiology 01/2014; · 3.48 Impact Factor

Publication Stats

2k Citations
568.07 Total Impact Points

Institutions

  • 2009–2014
    • University of British Columbia - Okanagan
      • • Faculty of Health and Social Development
      • • School of Health and Exercise Sciences
      Kelowna, British Columbia, Canada
  • 2013
    • University of British Columbia - Vancouver
      Vancouver, British Columbia, Canada
    • Government of British Columbia, Canada
      Vancouver, British Columbia, Canada
  • 2005–2013
    • University of Otago
      • Department of Physiology
      Dunedin, Otago, New Zealand
  • 2012
    • University of Sydney
      Sydney, New South Wales, Australia
  • 2008–2012
    • University of South Wales
      • Faculty of Health, Sport and Science
      Pontypridd, WLS, United Kingdom
  • 2011
    • University of Alberta
      • Faculty of Physical Education and Recreation
      Edmonton, Alberta, Canada
    • University of Brighton
      Brighton, England, United Kingdom
  • 2002–2011
    • Liverpool John Moores University
      • Research Institute for Sport and Exercise Sciences (RISES)
      Liverpool, ENG, United Kingdom
  • 2010
    • University of Lincoln
      • School of Social and Political Sciences
      Lincoln, ENG, United Kingdom
  • 2009–2010
    • Toyo University
      • Department of Biomedical Engineering
      Tōkyō, Japan
  • 2008–2010
    • University of Oxford
      • Department of Engineering Science
      Oxford, ENG, United Kingdom
  • 2008–2009
    • University of North Texas HSC at Fort Worth
      • Department of Integrative Physiology
      Fort Worth, TX, United States
  • 2007
    • University of Melbourne
      • Department of Zoology
      Melbourne, Victoria, Australia
    • Lincoln University New Zealand
      Lincoln, Canterbury Region, New Zealand
  • 2003–2005
    • The University of Calgary
      • Faculty of Medicine
      Calgary, Alberta, Canada