The Experts below are selected from a list of 231 Experts worldwide ranked by ideXlab platform

Craig G Crandall - One of the best experts on this subject based on the ideXlab platform.

  • cerebral vasomotor reactivity steady state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Craig G Crandall, Rebekah A. I. Lucas, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P < 0.01) and CVCI versus P ET , CO 2 (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2 is similar regardless of the employed methodology to induce changes in P aCO 2 and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

  • Cerebral vasomotor reactivity: steady‐state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Rebekah A. I. Lucas, Craig G Crandall, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P 

  • end tidal Carbon Dioxide Tension reflects arterial Carbon Dioxide Tension in the heat stressed human with and without simulated hemorrhage
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2011
    Co-Authors: Matthew S Ganio, Kimberly A Hubing, Jeffrey L Hastings, Craig G Crandall
    Abstract:

    End-tidal Carbon Dioxide Tension (PetCO2) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is depend...

  • the effects of reduced end tidal Carbon Dioxide Tension on cerebral blood flow during heat stress
    The Journal of Physiology, 2009
    Co-Authors: Kimberly A Hubing, Craig G Crandall, Jonathan E Wingo
    Abstract:

    Passive heat stress reduces arterial Carbon Dioxide partial pressure () as reflected by 3 to 5 Torr reductions in end-tidal Carbon Dioxide Tension (). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While is a strong regulator of CBVC, it is unlikely that the relatively small change in during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that , referenced by , is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), , middle cerebral artery blood velocity (MCA Vmean), and calculated CBVC (MCA Vmean/MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P= 0.55). Control heat stress increased internal temperature ∼1.3°C, which resulted in decreases in , MCA Vmean and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P= 0.31). Heat stress + clamp successfully restored to the normothermic level (P= 0.99) and increased MCA Vmean (P= 0.002) and CBVC (P= 0.008) relative to control heat stress. Despite restoration of , MCA Vmean (P= 0.005) and CBVC (P= 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in , as referenced by , contribute to the decrease in MCA Vmean and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.

Vincent Pellegrino - One of the best experts on this subject based on the ideXlab platform.

  • association between arterial Carbon Dioxide Tension and clinical outcomes in venoarterial extracorporeal membrane oxygenation
    Critical Care Medicine, 2020
    Co-Authors: Arne Diehl, Aidan J C Burrell, Peta M A Alexander, Peter Rycus, Ryan P Barbaro, Vincent Pellegrino
    Abstract:

    Objectives The manipulation of arterial Carbon Dioxide Tension is associated with differential mortality and neurologic injury in intensive care and cardiac arrest patients; however, few studies have investigated this relationship in patients on venoarterial extracorporeal membrane oxygenation. We investigated the association between the initial arterial Carbon Dioxide Tension and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiac arrest and refractory cardiogenic shock. Design Retrospective cohort analysis of adult patients recorded in the international Extracorporeal Life Support Organization Registry. Setting Data reported to the Extracorporeal Life Support Organization from all international extracorporeal membrane oxygenation centers during 2003-2016. Patients Adult patients (≥ 18 yr old) supported with venoarterial extracorporeal membrane oxygenation. Interventions None. Measurements and main results A total of 7,168 patients had sufficient data for analysis at the initiation of venoarterial extracorporeal membrane oxygenation, 4,918 of these patients had arterial Carbon Dioxide Tension data available at 24 hours on support. The overall in-hospital mortality rate was 59.9%. A U-shaped relationship between arterial Carbon Dioxide Tension Tension at extracorporeal membrane oxygenation initiation and in-hospital mortality was observed. Increased mortality was observed with a arterial Carbon Dioxide Tension less than 30 mm Hg (odds ratio, 1.26; 95% CI, 1.08-1.47; p = 0.003) and greater than 60 mm Hg (odds ratio, 1.28; 95% CI, 1.10-1.50; p = 0.002). Large reductions (> 20 mm Hg) in arterial Carbon Dioxide Tension over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outcome (odds ratio, 1.63; 95% CI, 1.03-2.59; p = 0.04), independent of the initial arterial Carbon Dioxide Tension. Conclusions Initial arterial Carbon Dioxide Tension Tension was independently associated with mortality in this cohort of venoarterial extracorporeal membrane oxygenation patients. Reductions in arterial Carbon Dioxide Tension (> 20 mm Hg) from the initiation of extracorporeal membrane oxygenation were associated with neurologic complications. Further prospective studies testing these associations are warranted.

  • Association Between Arterial Carbon Dioxide Tension and Clinical Outcomes in Venoarterial Extracorporeal Membrane Oxygenation.
    Critical Care Medicine, 2020
    Co-Authors: Arne Diehl, Peta M A Alexander, Peter Rycus, Ryan P Barbaro, Vincent Pellegrino, Aidan Burrell, David Pilcher
    Abstract:

    OBJECTIVES The manipulation of arterial Carbon Dioxide Tension is associated with differential mortality and neurologic injury in intensive care and cardiac arrest patients; however, few studies have investigated this relationship in patients on venoarterial extracorporeal membrane oxygenation. We investigated the association between the initial arterial Carbon Dioxide Tension and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiac arrest and refractory cardiogenic shock. DESIGN Retrospective cohort analysis of adult patients recorded in the international Extracorporeal Life Support Organization Registry. SETTING Data reported to the Extracorporeal Life Support Organization from all international extracorporeal membrane oxygenation centers during 2003-2016. PATIENTS Adult patients (≥ 18 yr old) supported with venoarterial extracorporeal membrane oxygenation. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS A total of 7,168 patients had sufficient data for analysis at the initiation of venoarterial extracorporeal membrane oxygenation, 4,918 of these patients had arterial Carbon Dioxide Tension data available at 24 hours on support. The overall in-hospital mortality rate was 59.9%. A U-shaped relationship between arterial Carbon Dioxide Tension Tension at extracorporeal membrane oxygenation initiation and in-hospital mortality was observed. Increased mortality was observed with a arterial Carbon Dioxide Tension less than 30 mm Hg (odds ratio, 1.26; 95% CI, 1.08-1.47; p = 0.003) and greater than 60 mm Hg (odds ratio, 1.28; 95% CI, 1.10-1.50; p = 0.002). Large reductions (> 20 mm Hg) in arterial Carbon Dioxide Tension over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outcome (odds ratio, 1.63; 95% CI, 1.03-2.59; p = 0.04), independent of the initial arterial Carbon Dioxide Tension. CONCLUSIONS Initial arterial Carbon Dioxide Tension Tension was independently associated with mortality in this cohort of venoarterial extracorporeal membrane oxygenation patients. Reductions in arterial Carbon Dioxide Tension (> 20 mm Hg) from the initiation of extracorporeal membrane oxygenation were associated with neurologic complications. Further prospective studies testing these associations are warranted.

Rong Zhang - One of the best experts on this subject based on the ideXlab platform.

  • cerebral vasomotor reactivity steady state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Craig G Crandall, Rebekah A. I. Lucas, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P < 0.01) and CVCI versus P ET , CO 2 (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2 is similar regardless of the employed methodology to induce changes in P aCO 2 and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

  • Cerebral vasomotor reactivity: steady‐state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Rebekah A. I. Lucas, Craig G Crandall, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P 

Arne Diehl - One of the best experts on this subject based on the ideXlab platform.

  • association between arterial Carbon Dioxide Tension and clinical outcomes in venoarterial extracorporeal membrane oxygenation
    Critical Care Medicine, 2020
    Co-Authors: Arne Diehl, Aidan J C Burrell, Peta M A Alexander, Peter Rycus, Ryan P Barbaro, Vincent Pellegrino
    Abstract:

    Objectives The manipulation of arterial Carbon Dioxide Tension is associated with differential mortality and neurologic injury in intensive care and cardiac arrest patients; however, few studies have investigated this relationship in patients on venoarterial extracorporeal membrane oxygenation. We investigated the association between the initial arterial Carbon Dioxide Tension and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiac arrest and refractory cardiogenic shock. Design Retrospective cohort analysis of adult patients recorded in the international Extracorporeal Life Support Organization Registry. Setting Data reported to the Extracorporeal Life Support Organization from all international extracorporeal membrane oxygenation centers during 2003-2016. Patients Adult patients (≥ 18 yr old) supported with venoarterial extracorporeal membrane oxygenation. Interventions None. Measurements and main results A total of 7,168 patients had sufficient data for analysis at the initiation of venoarterial extracorporeal membrane oxygenation, 4,918 of these patients had arterial Carbon Dioxide Tension data available at 24 hours on support. The overall in-hospital mortality rate was 59.9%. A U-shaped relationship between arterial Carbon Dioxide Tension Tension at extracorporeal membrane oxygenation initiation and in-hospital mortality was observed. Increased mortality was observed with a arterial Carbon Dioxide Tension less than 30 mm Hg (odds ratio, 1.26; 95% CI, 1.08-1.47; p = 0.003) and greater than 60 mm Hg (odds ratio, 1.28; 95% CI, 1.10-1.50; p = 0.002). Large reductions (> 20 mm Hg) in arterial Carbon Dioxide Tension over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outcome (odds ratio, 1.63; 95% CI, 1.03-2.59; p = 0.04), independent of the initial arterial Carbon Dioxide Tension. Conclusions Initial arterial Carbon Dioxide Tension Tension was independently associated with mortality in this cohort of venoarterial extracorporeal membrane oxygenation patients. Reductions in arterial Carbon Dioxide Tension (> 20 mm Hg) from the initiation of extracorporeal membrane oxygenation were associated with neurologic complications. Further prospective studies testing these associations are warranted.

  • Association Between Arterial Carbon Dioxide Tension and Clinical Outcomes in Venoarterial Extracorporeal Membrane Oxygenation.
    Critical Care Medicine, 2020
    Co-Authors: Arne Diehl, Peta M A Alexander, Peter Rycus, Ryan P Barbaro, Vincent Pellegrino, Aidan Burrell, David Pilcher
    Abstract:

    OBJECTIVES The manipulation of arterial Carbon Dioxide Tension is associated with differential mortality and neurologic injury in intensive care and cardiac arrest patients; however, few studies have investigated this relationship in patients on venoarterial extracorporeal membrane oxygenation. We investigated the association between the initial arterial Carbon Dioxide Tension and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiac arrest and refractory cardiogenic shock. DESIGN Retrospective cohort analysis of adult patients recorded in the international Extracorporeal Life Support Organization Registry. SETTING Data reported to the Extracorporeal Life Support Organization from all international extracorporeal membrane oxygenation centers during 2003-2016. PATIENTS Adult patients (≥ 18 yr old) supported with venoarterial extracorporeal membrane oxygenation. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS A total of 7,168 patients had sufficient data for analysis at the initiation of venoarterial extracorporeal membrane oxygenation, 4,918 of these patients had arterial Carbon Dioxide Tension data available at 24 hours on support. The overall in-hospital mortality rate was 59.9%. A U-shaped relationship between arterial Carbon Dioxide Tension Tension at extracorporeal membrane oxygenation initiation and in-hospital mortality was observed. Increased mortality was observed with a arterial Carbon Dioxide Tension less than 30 mm Hg (odds ratio, 1.26; 95% CI, 1.08-1.47; p = 0.003) and greater than 60 mm Hg (odds ratio, 1.28; 95% CI, 1.10-1.50; p = 0.002). Large reductions (> 20 mm Hg) in arterial Carbon Dioxide Tension over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outcome (odds ratio, 1.63; 95% CI, 1.03-2.59; p = 0.04), independent of the initial arterial Carbon Dioxide Tension. CONCLUSIONS Initial arterial Carbon Dioxide Tension Tension was independently associated with mortality in this cohort of venoarterial extracorporeal membrane oxygenation patients. Reductions in arterial Carbon Dioxide Tension (> 20 mm Hg) from the initiation of extracorporeal membrane oxygenation were associated with neurologic complications. Further prospective studies testing these associations are warranted.

Rebekah A. I. Lucas - One of the best experts on this subject based on the ideXlab platform.

  • cerebral vasomotor reactivity steady state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Craig G Crandall, Rebekah A. I. Lucas, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P < 0.01) and CVCI versus P ET , CO 2 (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2 is similar regardless of the employed methodology to induce changes in P aCO 2 and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

  • Cerebral vasomotor reactivity: steady‐state versus transient changes in Carbon Dioxide Tension
    Experimental Physiology, 2014
    Co-Authors: Rebekah A. I. Lucas, Craig G Crandall, Rong Zhang
    Abstract:

    New Findings What is the central question of this study? The relationship between changes in cerebral blood flow and arterial Carbon Dioxide Tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in Carbon Dioxide Tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia. What is the main finding and its importance? The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia. Cerebral vasomotor reactivity (CVMR) to changes in arterial Carbon Dioxide Tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal Carbon Dioxide Tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P