Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Lower Body Negative Pressure ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex ◽  
Underlying Mechanisms ◽  
End Tidal ◽  
Induced Changes ◽  
The Relationship

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA Vmean (middle cerebral artery mean blood velocity) and V̇E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO2 levels (0, 3.5 and 5% CO2). The regression line of the linear relationship between V̇E and PETCO2 (end-tidal CO2) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA Vmean and PETCO2 was not shifted by LBNP-induced changes in PETCO2. However, changes in V̇E from rest to LBNP were more related to changes in MCA Vmean than changes in PETCO2. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO2 from the brain causing hyperpnoea following activation of the central chemoreflex.

Manipulation of central blood volume and implications for respiratory control function

2014 ◽  
Vol 306 (12) ◽  
pp. H1669-H1678 ◽  
Author(s):  
Tadayoshi Miyamoto ◽  
Damian Miles Bailey ◽  
Hidehiro Nakahara ◽  
Shinya Ueda ◽  
Masashi Inagaki ◽  
...  
Keyword(s):  
Blood Volume ◽  
Lower Body Negative Pressure ◽  
Control Function ◽  
Minute Ventilation ◽  
Water Immersion ◽  
Respiratory Control ◽  
Intersection Point ◽  
Operating Point ◽  
Central Blood Volume ◽  
End Tidal

The respiratory operating point (ventilatory or arterial Pco2 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 Pco2 (PetCO2) and minute ventilation (V̇e) [V̇e = S × (PetCO2 − B)], whereas the plant was determined by the hyperbolic relationship between V̇e and PetCO2 (PetCO2 = A/V̇e + C). Changes in V̇e at the operating point were not observed under either WI or LBNP conditions despite altered PetCO2 ( 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 (PetCO2 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.

Cerebral critical closing pressure and CO2 responses during the progression toward syncope

2013 ◽  
Vol 114 (6) ◽  
pp. 801-807 ◽  
Author(s):  
K. A. Zuj ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
R. L. Hughson
Keyword(s):  
Lower Body Negative Pressure ◽  
Resistance Index ◽  
Bed Rest ◽  
Tolerance Test ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Cerebral Blood Velocity ◽  
End Tidal ◽  
Closing Pressure

Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BPMCA) and reductions in arterial CO2 as reflected by end-tidal values (PetCO2). It was hypothesized that reductions in PetCO2 increase cerebrovascular tone before a drop in BPMCA that ultimately leads to syncope. Twelve men (21–42 yr of age) completed an orthostatic tolerance test consisting of head-up tilt and progressive lower body negative pressure to presyncope, before and after completing 5 days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BPMCA, and PetCO2 were continuously recorded throughout the test. Cerebrovascular indicators, cerebrovascular resistance, critical closing pressure (CrCP), and resistance area product (RAP), were calculated. Comparing from supine baseline to 6–10 min after the start of tilt, there were reductions in CBFV, PetCO2, BPMCA, and CrCP, an increase in RAP, and no change in cerebrovascular resistance index. Over the final 15 min before syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in PetCO2 ( r = 0.69 ± 0.17 and r = 0.63 ± 0.20, respectively), and BPMCA, which was not reduced until the last minute of the test, was correlated with a reduction in RAP ( r = 0.91 ± 0.09). Post-HDBR, tilt tolerance was markedly reduced, and changes in CBFV were dominated by a greater reduction in BPMCA with no relationships to PetCO2. Therefore, pre-HDBR, changes in PetCO2 with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope, whereas, after 5 days of HDBR, orthostatic responses were dominated by changes in BPMCA.

Effect of CO2 on the ventilatory sensitivity to rising body temperature during exercise

2011 ◽  
Vol 110 (5) ◽  
pp. 1334-1341 ◽  
Author(s):  
Keiji Hayashi ◽  
Yasushi Honda ◽  
Natsuki Miyakawa ◽  
Naoto Fujii ◽  
Masashi Ichinose ◽  
...  
Keyword(s):  
Body Temperature ◽  
Prolonged Exercise ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cycle Ergometer ◽  
Blood Velocity ◽  
Esophageal Temperature ◽  
Arterial Blood ◽  
End Tidal ◽  
Respiratory Gases

We examined the degree to which ventilatory sensitivity to rising body temperature (the slope of the regression line relating ventilation and body temperature) is altered by restoration of arterial Pco2 to the eucapnic level during prolonged exercise in the heat. Thirteen subjects exercised for ∼60 min on a cycle ergometer at 50% of peak O2 uptake with and without inhalation of CO2-enriched air. Subjects began breathing CO2-enriched air at the point that end-tidal Pco2 started to decline. Esophageal temperature (Tes), minute ventilation (V̇e), tidal volume (VT), respiratory frequency ( fR), respiratory gases, middle cerebral artery blood velocity, and arterial blood pressure were recorded continuously. When V̇e, VT, fR, and ventilatory equivalents for O2 uptake (V̇e/V̇o2) and CO2 output (V̇e/V̇co2) were plotted against changes in Tes from the start of the CO2-enriched air inhalation (ΔTes), the slopes of the regression lines relating V̇e, VT, V̇e/V̇o2, and V̇e/V̇co2 to ΔTes (ventilatory sensitivity to rising body temperature) were significantly greater when subjects breathed CO2-enriched air than when they breathed room air (V̇e: 19.8 ± 10.3 vs. 8.9 ± 6.7 l·min−1·°C−1, VT: 18 ± 120 vs. −81 ± 92 ml/°C; V̇e/V̇o2: 7.4 ± 5.5 vs. 2.6 ± 2.3 units/°C, and V̇e/V̇co2: 7.6 ± 6.6 vs. 3.4 ± 2.8 units/°C). The increase in V̇e was accompanied by increases in VT and fR. These results suggest that restoration of arterial Pco2 to nearly eucapnic levels increases ventilatory sensitivity to rising body temperature by around threefold.

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex

scholarly journals The cerebrovascular response to lower-body negative pressure vs. head-up tilt

2017 ◽  
Vol 122 (4) ◽  
pp. 877-883 ◽  
Author(s):  
Anne-Sophie G. T. Bronzwaer ◽  
Jasper Verbree ◽  
Wim J. Stok ◽  
Mat J. A. P. Daemen ◽  
Mark A. van Buchem ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Negative Pressure ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Head Up Tilt ◽  
End Tidal ◽  
Pronounced Reduction

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (−50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBF v) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT ( P ≤ 0.020). Mean CBF v initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller ( P ≤ 0.029) during LBNP. The reduction in end-tidal Pco2 partial pressure (PetCO2) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT ( P = 0.008). We consider the larger decrease in CBF v during HUT vs. LBNP attributable to the pronounced reduction in PetCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality. NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.

Efficacy of nifedipine to prevent systemic and renal vasoconstrictor effects of endothelin

1990 ◽  
Vol 259 (2) ◽  
pp. F304-F311 ◽  
Author(s):  
P. Madeddu ◽  
X. P. Yang ◽  
V. Anania ◽  
C. Troffa ◽  
A. Pazzola ◽  
...  
Keyword(s):  
Bolus Injection ◽  
Regression Line ◽  
The Other ◽  
Base Line ◽  
Intravenous Bolus ◽  
Ang Ii ◽  
Hemodynamic Parameters ◽  
Renal Vasoconstriction ◽  
Induced Changes ◽  
The Relationship

We investigated whether systemic and renal vasoconstriction induced by porcine endothelin (endothelin 1) is prevented by nifedipine in awake normotensive rats. Endothelin (0.07-1.4 nmol/kg iv) induced a long-lasting increase in mean blood pressure (MBP) and a decrease in renal blood flow (RBF). Maximal decrease in RBF was 25 +/- 7% (0.07 nmol/kg), 40 +/- 2 (0.35), 67 +/- 5 (0.70), and 74 +/- 8 (1.4). Hemodynamic parameters were back to base line within 35 +/- 5 min (0.07 nmol/kg), 43 +/- 6 (0.35), 60 +/- 4 (0.70), and 81 +/- 7 (1.4). Intravenous bolus injection of either angiotensin II (ANG II, 0.006-0.024 nmol/kg) or norepinephrine (0.40-1.60 nmol/kg) caused a dose-related short-lasting increase in MBP and a decrease in RBF. Endothelin was less potent than ANG II (1:3.42) and more potent than norepinephrine (1:0.015) as a renal vasoconstrictor. Nifedipine (1 mg/kg ip) was equally effective in preventing the increase in MBP caused by endothelin, norepinephrine, or ANG II. It exerted a weaker protection on the renal hemodynamic response to endothelin compared with the inhibition of the other two vasoconstrictors. Thus the regression line representing the relationship between endothelin-induced changes in MBP and RBF was steeper in rats given nifedipine (slope: vehicle, -1.33; nifedipine, -5.50; P less than 0.05). These studies suggest that nifedipine can partially prevent systemic and renal vasoconstriction caused by exogenously administered endothelin in awake normotensive rats.

Cerebral hemodynamics during orthostatic stress assessed by nonlinear modeling

2006 ◽  
Vol 101 (1) ◽  
pp. 354-366 ◽  
Author(s):  
Georgios D. Mitsis ◽  
Rong Zhang ◽  
Benjamin D. Levine ◽  
Vasilis Z. Marmarelis
Keyword(s):  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Nonlinear Modeling ◽  
Cerebral Hemodynamics ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Cerebrovascular Reserve ◽  
Vasomotor Reactivity ◽  
Arterial Blood ◽  
Cerebral Vasomotor Reactivity

The effects of orthostatic stress, induced by lower body negative pressure (LBNP), on cerebral hemodynamics were examined in a nonlinear context. Spontaneous fluctuations of beat-to-beat mean arterial blood pressure (MABP) in the finger, mean cerebral blood flow velocity (MCBFV) in the middle cerebral artery, as well as breath-by-breath end-tidal CO2 concentration (PetCO2) were measured continuously in 10 healthy subjects under resting conditions and during graded LBNP to presyncope. A two-input nonlinear Laguerre-Volterra network model was employed to study the dynamic effects of MABP and PetCO2 changes, as well as their nonlinear interactions, on MCBFV variations in the very low (VLF; below 0.04 Hz), low (LF; 0.04–0.15 Hz), and high frequency (HF; 0.15–0.30 Hz) ranges. Dynamic cerebral autoregulation was described by the model terms corresponding to MABP, whereas cerebral vasomotor reactivity was described by the model PetCO2 terms. The nonlinear model terms reduced the output prediction normalized mean square error substantially (by 15–20%) and had a prominent effect in the VLF range, both under resting conditions and during LBNP. Whereas MABP fluctuations dominated in the HF range and played a significant role in the VLF and LF ranges, changes in PetCO2 accounted for a considerable fraction of the VLF and LF MCBFV variations, especially at high LBNP levels. The magnitude of the linear and nonlinear MABP-MCBFV Volterra kernels increased substantially above −30 mmHg LBNP in the VLF range, implying impaired dynamic autoregulation. In contrast, the magnitude of the PetCO2-MCBFV kernels reduced during LBNP at all frequencies, suggesting attenuated cerebral vasomotor reactivity under dynamic conditions. We speculate that these changes may reflect a progressively reduced cerebrovascular reserve to compensate for the increasingly unstable systemic circulation during orthostatic stress that could ultimately lead to cerebral hypoperfusion and syncope.

Detection of Hypercapnia by Normal Subjects

1987 ◽  
Vol 73 (3) ◽  
pp. 333-335 ◽  
Author(s):  
R. M. Schwartzstein ◽  
K. La Hive ◽  
A. Pope ◽  
R. A. Steinbrook ◽  
D. E. Leith ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Pulmonary Ventilation ◽  
Control Period ◽  
Feedback System ◽  
Normal Subjects ◽  
Test Period ◽  
Absolute Level ◽  
End Tidal ◽  
Induced Changes ◽  
Different Levels

1. To investigate whether changes in Paco2 can be detected independently of the CO2-induced changes in pulmonary ventilation, we tested five normal subjects for the ability to distinguish different levels of end-tidal Pco2 (PETco2) while holding minute ventilation constant. 2. Helped by a visual feedback system, the subjects maintained a constant ventilation targeted at a level that was higher than that dictated by the chemical drive at PETco2 = 50 mmHg (6.7 kPa). End-tidal Pco2 was held at 40 mmHg (5.3 kPa) during the first 2 min of each test trial ('control period'); then, for 4 min ('test period'), PETco2 was either elevated to 50 mmHg or kept at 40 mmHg. Twelve runs were performed by each subject. 3. In 24 out of the total 30 trials (80%) in which PETco2 was raised during the test period to 50 mmHg, the subjects detected the changes. There was one false positive result (3%), when PETco2 kept at 40 mmHg during the test period was reported as different from control. In four out of the five subjects the ability to detect the change in PETco2 from 40 to 50 mmHg was statistically significant. 4. We conclude that increases in PETco2 can be detected independently of changes in the absolute level of ventilation.

Effects of CO2 breathing on ventilatory response to sustained hypoxia in normal adults

1989 ◽  
Vol 66 (3) ◽  
pp. 1071-1078 ◽  
Author(s):  
D. Georgopoulos ◽  
D. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Inhibitory Effect ◽  
Hypoxic Exposure ◽  
Initial Increase ◽  
Co2 Levels ◽  
End Tidal ◽  
The Relationship ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Co2

The relationship between CO2 and ventilatory response to sustained hypoxia was examined in nine normal young adults. At three different levels of end-tidal partial pressure of CO2 (PETCO2, approximately 35, 41.8, and 44.3 Torr), isocapnic hypoxia was induced for 25 min and after 7 min of breathing 21% O2, isocapnic hypoxia was reinduced for 5 min. Regardless of PETCO2 levels, the ventilatory response to sustained hypoxia was biphasic, characterized by an initial increase (acute hypoxic response, AHR), followed by a decline (hypoxic depression). The biphasic response pattern was due to alteration in tidal volume, which at all CO2 levels decreased significantly (P less than 0.05), without a significant change in breathing frequency. The magnitude of the hypoxic depression, independent of CO2, correlated significantly (r = 0.78, P less than 0.001) with the AHR, but not with the ventilatory response to CO2. The decline of minute ventilation was not significantly affected by PETCO2 [averaged 2.3 +/- 0.6, 3.8 +/- 1.3, and 4.5 +/- 2.2 (SE) 1/min for PETCO2 35, 41.8, and 44.3 Torr, respectively]. This decay was significant for PETCO2 35 and 41.8 Torr but not for 44.3 Torr. The second exposure to hypoxia failed to elicit the same AHR as the first exposure; at all CO2 levels the AHR was significantly greater (P less than 0.05) during the first hypoxic exposure than during the second. We conclude that hypoxia exhibits a long-lasting inhibitory effect on ventilation that is independent of CO2, at least in the range of PETCO2 studied, but is related to hypoxic ventilatory sensitivity.

Response to hypercapnia and exercise hyperpnea in graded anesthesia

1984 ◽  
Vol 57 (6) ◽  
pp. 1796-1802 ◽  
Author(s):  
T. Chonan ◽  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Exercise Hyperpnea ◽  
Sciatic Nerves ◽  
End Tidal ◽  
Response To Exercise ◽  
The Relationship ◽  
End Tidal Co2 ◽  
Rebreathing Method

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)

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