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  • 1
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    Onset responses of ventilation and cerebral blood flow to hypercapnia in humans: rest and exercise
    American Physiological Society ; 2009
    In:  Journal of Applied Physiology Vol. 106, No. 3 ( 2009-03), p. 880-886
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 106, No. 3 ( 2009-03), p. 880-886
    Abstract: The respiratory and cerebrovascular reactivity to changes in arterial Pco 2 ([Formula: see text]) is an important mechanism that maintains CO 2 or pH homeostasis in the brain. It remains unclear, however, how cerebrovascular CO 2 reactivity might influence the respiratory chemoreflex. The purpose of the present study was therefore to examine the interaction between onset responses of the respiratory chemoreflex and middle cerebral artery (MCA) mean blood velocity ( V mean ) to hypercapnia (5.0% CO 2 -40% O 2 -balance N 2 ) at rest and during dynamic exercise (∼1.0 l/min O 2 consumption). Each onset response was evaluated using a single-exponential regression model consisting of the response time latency [CO 2 -response delay ( t 0 )] and time constant (τ). At rest, t 0 and τ data indicated that the MCA V mean onset response was faster than the ventilatory (V̇e) response ( P 〈 0.001). In contrast, during exercise, t 0 of V̇e and MCA V mean onset responses were decreased. In addition, despite the enhanced [Formula: see text] response to CO 2 administration ( P = 0.014), τ of MCA V mean tended to increase during exercise ( P = 0.054), whereas τ of V̇e decreased ( P = 0.015). These findings indicate that 1) at rest, faster washout of CO 2 via cerebral vasodilation results in a reduced activation of the central chemoreflex and subsequent reduced V̇e onset response, and 2) during exercise, despite higher rates of increasing [Formula: see text], the lack of change in the onset response of cerebral blood flow and reduced washout of CO 2 may act to augment the V̇e onset response.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.91292.2008
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1404365-8
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  • 2
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    The effect of oxygen on dynamic cerebral autoregulation: critical role of hypocapnia
    American Physiological Society ; 2010
    In:  Journal of Applied Physiology Vol. 108, No. 3 ( 2010-03), p. 538-543
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 108, No. 3 ( 2010-03), p. 538-543
    Abstract: Hypoxia is known to impair cerebral autoregulation (CA). Previous studies indicate that CA is profoundly affected by cerebrovascular tone, which is largely determined by the partial pressure of arterial O 2 and CO 2 . However, hypoxic-induced hyperventilation via respiratory chemoreflex activation causes hypocapnia, which may influence CA independent of partial pressure of arterial O 2 . To identify the effect of O 2 on dynamic cerebral blood flow regulation, we examined the influence of normoxia, isocapnia hyperoxia, hypoxia, and hypoxia with consequent hypocapnia on dynamic CA. We measured heart rate, blood pressure, ventilatory parameters, and middle cerebral artery blood velocity (transcranial Doppler). Dynamic CA was assessed ( n = 9) during each of four randomly assigned respiratory interventions: 1) normoxia (21% O 2 ); 2) isocapnic hyperoxia (40% O 2 ); 3) isocapnic hypoxia (14% O 2 ); and 4) hypocapnic hypoxia (14% O 2 ). During each condition, the rate of cerebral regulation (RoR), an established index of dynamic CA, was estimated during bilateral thigh cuff-induced transient hypotension. The RoR was unaltered during isocapnic hyperoxia. Isocapnic hypoxia attenuated the RoR (0.202 ± 0.003/s; 27%; P = 0.043), indicating impairment in dynamic CA. In contrast, hypocapnic hypoxia increased RoR (0.444 ± 0.069/s) from normoxia (0.311 ± 0.054/s; +55%; P = 0.041). These findings indicated that hypoxia disrupts dynamic CA, but hypocapnia augments the dynamic CA response. Because hypocapnia is a consequence of hypoxic-induced chemoreflex activation, it may provide a teleological means to effectively maintain dynamic CA in the face of prevailing arterial hypoxemia.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01235.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1404365-8
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  • 3
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    Hyperthermia modulates regional differences in cerebral blood flow to changes in CO 2
    American Physiological Society ; 2014
    In:  Journal of Applied Physiology Vol. 117, No. 1 ( 2014-07-01), p. 46-52
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 117, No. 1 ( 2014-07-01), p. 46-52
    Abstract: The purpose of this study was to assess blood flow responses to changes in carbon dioxide (CO 2 ) in the internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) during normothermic and hyperthermic conditions. Eleven healthy subjects aged 22 ± 2 (SD) yr were exposed to passive whole body heating followed by spontaneous hypocapnic and hypercapnic challenges in normothermic and hyperthermic conditions. Right ICA, ECA, and VA blood flows, as well as left middle cerebral artery (MCA) mean blood velocity ( V mean ), were measured. Esophageal temperature was elevated by 1.53 ± 0.09°C before hypocapnic and hypercapnic challenges during heat stress. Whole body heating increased ECA blood flow and cardiac output by 130 ± 78 and 47 ± 26%, respectively ( P 〈 0.001), while blood flow (or velocity) in the ICA, MCA, and VA was reduced by 17 ± 14, 24 ± 18, and 12 ± 7%, respectively ( P 〈 0.001). Regardless of the thermal conditions, ICA and VA blood flows and MCA V mean were decreased by hypocapnic challenges and increased by hypercapnic challenges. Similar responses in ECA blood flow were observed in hyperthermia but not in normothermia. Heat stress did not alter CO 2 reactivity in the MCA and VA. However, CO 2 reactivity in the ICA was decreased (3.04 ± 1.17 vs. 2.23 ± 1.03%/mmHg; P = 0.039) but that in the ECA was enhanced (0.45 ± 0.47 vs. 0.95 ± 0.61%/mmHg; P = 0.032). These results indicate that hyperthermia is capable of altering dynamic cerebral blood flow regulation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01078.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1404365-8
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  • 4
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    Dynamic cerebral autoregulation during cognitive task: effect of hypoxia
    American Physiological Society ; 2018
    In:  Journal of Applied Physiology Vol. 124, No. 6 ( 2018-06-01), p. 1413-1419
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 124, No. 6 ( 2018-06-01), p. 1413-1419
    Abstract: Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O 2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA V mean ) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA V mean increased during the cognitive activity ( P 〈 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P 〈 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O 2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA V mean relationship. NEW & NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O 2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00909.2017
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1404365-8
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  • 5
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    The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension
    American Physiological Society ; 2015
    In:  Journal of Applied Physiology Vol. 119, No. 5 ( 2015-09-01), p. 527-533
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 119, No. 5 ( 2015-09-01), p. 527-533
    Abstract: The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; −50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s −1 , P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation ( P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol ( P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00277.2015
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1404365-8
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  • 6
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    Effects of acute hypoxia on human cognitive processing: a study using ERPs and SEPs
    American Physiological Society ; 2017
    In:  Journal of Applied Physiology Vol. 123, No. 5 ( 2017-11-01), p. 1246-1255
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 123, No. 5 ( 2017-11-01), p. 1246-1255
    Abstract: Although hypoxia has the potential to impair the cognitive function, the effects of acute hypoxia on the high-order brain function (executive and/or inhibitory processing) and somatosensory ascending processing remain unknown. We tested the hypothesis that acute hypoxia impairs both motor executive and inhibitory processing and somatosensory ascending processing. Fifteen healthy subjects performed two sessions ( sessions 1 and 2), consisting of electroencephalographic event-related potentials with somatosensory Go/No-go paradigms and somatosensory-evoked potentials (SEPs) under two conditions (hypoxia and normoxia) on different days. On 1 day, participants breathed room air in the first and second sessions of the experiment; on the other day, participants breathed room air in the first session, and 12% O 2 in the second session. Acute hypoxia reduced the peak amplitudes of Go-P300 and No-go-P300, and delayed the peak latency of Go-P300. However, no significant differences were observed in the peak amplitude or latency of N140, behavioral data, or the amplitudes and latencies of individual SEP components between the two conditions. These results suggest that acute hypoxia impaired neural activity in motor executive and inhibitory processing, and delayed higher cognitive processing for motor execution, whereas neural activity in somatosensory processing was not affected by acute hypoxia. NEW & NOTEWORTHY Hypoxia has the potential to impair the cognitive function, but the effects of acute hypoxia on the cognitive function remain debatable. We investigated the effects of acute hypoxia on human cognitive processing using electroencephalographic event-related potentials and somatosensory-evoked potentials. Acute normobaric hypoxia impaired neural activity in motor executive and inhibitory processing, but no significant differences were observed in neural activity in somatosensory processing.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00348.2017
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1404365-8
    SSG: 12
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  • 7
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    Therapeutic inhibition of microRNA-34a ameliorates aortic valve calcification via modulation of Notch1-Runx2 signalling
    Oxford University Press (OUP) ; 2019
    In:  Cardiovascular Research ( 2019-08-29)
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), ( 2019-08-29)
    Abstract: Calcific aortic valve stenosis (CAVS) is the most common valvular heart disease and is increased with elderly population. However, effective drug therapy has not been established yet. This study aimed to investigate the role of microRNAs (miRs) in the development of CAVS. Methods and results We measured the expression of 10 miRs, which were reportedly involved in calcification by using human aortic valve tissue from patients who underwent aortic valve replacement with CAVS or aortic regurgitation (AR) and porcine aortic valve interstitial cells (AVICs) after treatment with osteogenic induction medium. We investigated whether a specific miR-inhibitor can suppress aortic valve calcification in wire injury CAVS mice model. Expression of miR-23a, miR-34a, miR-34c, miR-133a, miR-146a, and miR-155 was increased, and expression of miR-27a and miR-204 was decreased in valve tissues from CAVS compared with those from AR. Expression of Notch1 was decreased, and expression of Runt-related transcription factor 2 (Runx2) was increased in patients with CAVS compared with those with AR. We selected miR-34a among increased miRs in porcine AVICs after osteogenic treatment, which was consistent with results from patients with CAVS. MiR-34a increased calcium deposition in AVICs compared with miR-control. Notch1 expression was decreased, and Runx2 expression was increased in miR-34a transfected AVICs compared with that in miR-control. Conversely, inhibition of miR-34a significantly attenuated these calcification signals in AVICs compared with miR-control. RNA pull-down assay revealed that miR-34a directly targeted Notch1 expression by binding to Notch1 mRNA 3′ untranslated region. In wire injury CAVS mice, locked nucleic acid miR-34a inhibitor suppressed aortic velocity, calcium deposition of aortic valves, and cardiac hypertrophy, which were involved in decreased Runx2 and increased Notch1 expressions. Conclusion miR-34a plays an important role in the development of CAVS via Notch1–Runx2 signalling pathway. Inhibition of miR-34a may be the therapeutic target for CAVS.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvz210
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1499917-1
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  • 8
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    Diverse effects of phospholipids on lipoprotein sorting and ATP hydrolysis by the ABC transporter LolCDE complex
    Elsevier BV ; 2007
    In:  Biochimica et Biophysica Acta (BBA) - Biomembranes Vol. 1768, No. 7 ( 2007-07), p. 1848-1854
    Details
    In: Biochimica et Biophysica Acta (BBA) - Biomembranes, Elsevier BV, Vol. 1768, No. 7 ( 2007-07), p. 1848-1854
    Type of Medium: Online Resource
    ISSN: 0005-2736
    URL: Article
    DOI: 10.1016/j.bbamem.2007.04.005
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 2209384-9
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  • 9
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    Interaction between the ventilatory and cerebrovascular responses to hypo‐ and hypercapnia at rest and during exercise
    Wiley ; 2008
    In:  The Journal of Physiology Vol. 586, No. 17 ( 2008-09), p. 4327-4338
    Details
    In: The Journal of Physiology, Wiley, Vol. 586, No. 17 ( 2008-09), p. 4327-4338
    Abstract: Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide ( P ) via limiting changes in brain [H + ] modulates ventilatory control. It remains unclear, however, how exercise‐induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO 2 . The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise‐induced alterations in ventilatory chemoreflex on cerebrovascular CO 2 reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO 2 reactivity were evaluated ( n = 7) by the administration of CO 2 as well as by voluntary hypo‐ and hyperventilation at rest and during steady‐state exercise. During exercise, in the central controller, the regression line for the P –minute ventilation relation shifted to higher and P with no change in gain ( P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (−4.1 ± 0.8 to −2.0 ± 0.2 mmHg l −1 min −1 , P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (−8.0 ± 2.3 to −3.5 ± 1.0 U, P = 0.02). In contrast, cerebrovascular CO 2 reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 ± 0.2 to 2.8 ± 0.2% mmHg −1 , P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO 2 homeostasis in the brain during exercise.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2008.157073
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 1475290-6
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  • 10
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    Manipulation of central blood volume and implications for respiratory control function
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 306, No. 12 ( 2014-06-15), p. H1669-H1678
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 306, No. 12 ( 2014-06-15), p. H1669-H1678
    Abstract: The respiratory operating point (ventilatory or arterial Pco 2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal Pco 2 (Pet CO 2 ) and minute ventilation (V̇e) [V̇e = S × (Pet CO 2 − B)], whereas the plant was determined by the hyperbolic relationship between V̇e and Pet CO 2 (Pet CO 2 = A/V̇e + C). Changes in V̇e at the operating point were not observed under either WI or LBNP conditions despite altered Pet CO 2 ( P 〈 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (Pet CO 2 intercept B) rightward and leftward, respectively ( P 〈 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00987.2013
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477308-9
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