Effects of changes in central blood volume on carotid-vasomotor baroreflex sensitivity at rest and during exercise

2006 ◽  
Vol 101 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Shigehiko Ogoh ◽  
R. Matthew Brothers ◽  
Quinton Barnes ◽  
Wendy L. Eubank ◽  
Megan N. Hawkins ◽  
...  
Keyword(s):  
Blood Volume ◽  
Baroreflex Sensitivity ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Central Blood Volume ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Maximal Gain ◽  
Neck Pressure ◽  
The Relationship

The purpose of this investigation was to examine whether the effect of changes in central blood volume on carotid-vasomotor baroreflex sensitivity at rest was the same during exercise. Eight men (means ± SE: age 26 ± 1 yr; height 180 ± 3 cm; weight 86 ± 6 kg) participated in the present study. Sixteen Torr of lower body negative pressure (LBNP) were applied to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak O2 uptake (104 ± 20 W). Subsequently, infusions of 25% human serum albumin solution were administered to increase CVP at rest and during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, the maximal gain (Gmax) of the carotid-vasomotor baroreflex function curve was measured using the neck pressure and neck suction technique. LBNP reduced CVP and increased the Gmax of the carotid-vasomotor baroreflex function curve at rest (+63 ± 25%, P = 0.006) and during exercise (+69 ± 19%, P = 0.002). In contrast to the LBNP, increases in CVP resulted in the Gmax of the carotid-vasomotor baroreflex function curve being decreased at rest −8 ± 4% and during exercise −18 ± 5% ( P > 0.05). These findings indicate that the relationship between CVP and carotid-vasomotor baroreflex sensitivity was nonlinear at rest and during exercise and suggests a saturation load of the cardiopulmonary baroreceptors at which carotid-vasomotor baroreflex sensitivity remains unchanged.

Central blood volume and blood pressure in conscious primates

1988 ◽  
Vol 254 (4) ◽  
pp. H693-H701 ◽  
Author(s):  
K. G. Cornish ◽  
J. P. Gilmore ◽  
T. McCulloch
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood

Conscious intact (I) and sinoaortic-denervated monkeys (SAD) were studied to determine the extent to which high-pressure receptors contribute to the maintenance of arterial blood pressure (BP) when venous return is decreased by hemorrhage (H) or lower body negative pressure (LBNP). In the I animals, mean BP did not decrease significantly until 5% of the estimated blood volume (EBV) was removed, whereas, with sinoaortic denervation, mean BP decreased significantly when less than 2% of EBV was removed. Left atrial pressure (LAP) decreased similarly in both groups of animals. In the I group during LBNP, mean BP did not change significantly, whereas pulse pressure decreased significantly when LBNP was decreased to -5 cmH2O. In the SAD animals, mean BP decreased significantly at an LBNP of -2 cmH2O, and at -5 cmH2O mean BP declined from 134.1 +/- 4 to 102.7 +/- 7 mmHg. LAP decreased similarly in both groups of animals. The data support the view that a nonhypotensive reduction in venous return unloads arterial baroreceptors sufficiently to activate the arterial baroreflex, probably through reductions in pulse pressure. In addition, low-pressure receptors by themselves do not appear to contribute importantly to blood pressure maintenance when venous return is decreased by either LBNP or a nonhypotensive hemorrhage.

scholarly journals Healthy older humans exhibit augmented carotid-cardiac baroreflex sensitivity with aspirin during muscle mechanoreflex and metaboreflex activation

2015 ◽  
Vol 309 (8) ◽  
pp. H1361-H1369 ◽  
Author(s):  
Rachel C. Drew ◽  
Cheryl A. Blaha ◽  
Michael D. Herr ◽  
Sean D. Stocker ◽  
Lawrence I. Sinoway
Keyword(s):  
Baroreflex Sensitivity ◽  
Low Dose ◽  
Voluntary Contraction ◽  
Operating Point ◽  
Arterial Blood ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Muscle Mechanoreflex ◽  
Maximal Gain ◽  
Neck Pressure

Low-dose aspirin inhibits thromboxane production and augments the sensitivity of carotid baroreflex (CBR) control of heart rate (HR) during concurrent muscle mechanoreflex and metaboreflex activation in healthy young humans. However, it is unknown how aging affects this response. Therefore, the effect of low-dose aspirin on carotid-cardiac baroreflex sensitivity during muscle mechanoreflex with and without metaboreflex activation in healthy older humans was examined. Twelve older subjects (6 men and 6 women, mean age: 62 ± 1 yr) performed two trials during two visits preceded by 7 days of low-dose aspirin (81 mg) or placebo. One trial involved 3 min of passive calf stretch (mechanoreflex) during 7.5 min of limb circulatory occlusion (CO). In another trial, CO was preceded by 1.5 min of 70% maximal voluntary contraction isometric calf exercise (mechanoreflex and metaboreflex). HR (ECG) and mean arterial blood pressure (MAP; Finometer) were recorded. CBR function was assessed using rapid neck pressure application (+40 to −80 mmHg). Aspirin significantly decreased baseline thromboxane B2 production by 83 ± 4% ( P < 0.05) but did not affect 6-keto-PGF1α. After aspirin, CBR-HR maximal gain and operating point gain were significantly higher during stretch with metabolite accumulation compared with placebo (maximal gain: −0.23 ± 0.03 vs. −0.14 ± 0.02 and operating point gain: −0.11 ± 0.03 vs. −0.04 ± 0.01 beats·min−1·mmHg−1 for aspirin and placebo, respectively, P < 0.05). In conclusion, these findings suggest that low-dose aspirin augments CBR-HR sensitivity during concurrent muscle mechanoreflex and metaboreflex activation in healthy older humans. This increased sensitivity appears linked to reduced thromboxane sensitization of muscle mechanoreceptors, which consequently improves CBR-HR control.

Cardiovascular and renal function during exercise-induced blood volume expansion in men

1994 ◽  
Vol 76 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
C. M. Gillen ◽  
T. Nishiyasu ◽  
G. Langhans ◽  
C. Weseman ◽  
G. W. Mack ◽  
...  
Keyword(s):  
Renal Function ◽  
Blood Volume ◽  
Lower Body Negative Pressure ◽  
Excretion Rate ◽  
Plasma Aldosterone ◽  
Direct Result ◽  
Intense Exercise ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Exercise Induced

To test the hypothesis that reduced baroreflex sensitivity is a direct result of exercise, we measured forearm vascular conductance (FVC) responses to graded lower body negative pressure (LBNP) 2, 20, and 44 h after intense exercise. Eight 4-min bouts of exercise at 85% of maximum oxygen uptake produced 3.5 +/- 0.7 and 3.9 +/- 1.0% blood volume (BV) expansions at 20 and 44 h of recovery, respectively. BV was unchanged from control values 2 h after exercise. The reduction in FVC was significantly less than control values during 30 and 40 mmHg of LBNP at 2 and 20 h of recovery, respectively, whereas heart rate and cardiac stroke volume responses were unchanged. Thus, a reduced FVC response to LBNP preceded BV expansion, demonstrating that exercise itself can elicit an attenuation of baroreflex function. To test the hypothesis that volume sensitivity of renal function is attenuated by intense exercise, we measured cardiovascular variables, plasma hormone concentrations, and renal output. At 20 h of recovery, resting mean arterial blood pressure and cardiac output were increased by 6 +/- 1 mmHg and 0.6 +/- 0.2 l/min, respectively, but resting plasma aldosterone and overnight Na+ excretion rate were unchanged. At 44 h of recovery, plasma aldosterone was decreased by 26 +/- 9% and overnight Na+ excretion rate was increased by 51 +/- 26%. Thus, appropriate endocrine and renal responses to increased BV were delayed until 44 h of recovery. Our findings suggest that a postexercise attenuation of baroreflex function participates in the induction of BV expansion by intense exercise.

Arterial and cardiopulmonary baroreflexes in 60- to 69- vs. 18- to 36-yr-old humans

1996 ◽  
Vol 80 (6) ◽  
pp. 1903-1910 ◽  
Author(s):  
X. Shi ◽  
K. M. Gallagher ◽  
R. M. Welch-O'Connor ◽  
B. H. Foresman
Keyword(s):  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Age Groups ◽  
Baroreflex Function ◽  
Carotid Baroreflex ◽  
Cardiopulmonary Baroreflex ◽  
Young Subjects ◽  
Neck Pressure ◽  
Cardiopulmonary Baroreceptors ◽  
Cardiovascular Variables

This study was designed to test the hypothesis that aging diminished baroreflex function during central hypovolemia. Eleven healthy young and eleven older (age 60-69 yr) individuals were assessed by using heart rate (HR) and mean arterial pressure (MAP) responses to neck pressure and suction during rest and lower body negative pressure (LBNP) of -15 Torr. The slope of forearm vascular resistance to central venous pressure during low-level LBNP was assessed as the index of cardiopulmonary baroreflex sensitivity. Baseline cardiovascular variables were not significantly different between the groups. In addition, there was no group difference in cardiopulmonary baroreflex (-3.6 vs. -3.7 units/mmHg for young vs. older, respectively) or carotid baroreflex (-0.39 vs. -0.35 beats.min-1.mmHg-1 and -0.26 vs. -0.35 mmHg/mmHg, for young vs. older, respectively) sensitivity. LBNP did not affect either HR or MAP, whereas it decreased CVP and increased FVR in both groups. LBNP significantly augmented the carotid-HR (-0.47 +/- 0.03 beats.min-1.mmHg-1) and carotid-MAP (-0.42 +/- 0.04 mmHg/mmHg) reflex gains in the young subjects only. We concluded that there was no difference in the discrete baroreflex function between the two age groups; however, the interaction of cardiopulmonary baroreceptors with carotid baroreflex function was absent in the older subjects, suggesting that the central integration of afferent neural inputs from the discrete baroreceptors was altered with aging.

Hemodilution, central blood volume, and renal responses after an isotonic saline infusion in humans

1997 ◽  
Vol 272 (2) ◽  
pp. R549-R556 ◽  
Author(s):  
L. B. Johansen ◽  
P. Bie ◽  
J. Warberg ◽  
N. J. Christensen ◽  
M. Hammerum ◽  
...  
Keyword(s):  
Blood Volume ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Plasma Norepinephrine ◽  
Central Blood Volume ◽  
Plasma Aldosterone Concentration ◽  
Renal Responses

To test the hypothesis that hemodilution is a mediator of the renal responses to an isotonic saline infusion in the supine position, eight males underwent 1) intravenous infusion of 1.5 liter of saline over 21 min (Saline), 2) infusion of 1.5 liter of saline in combination with lower body negative pressure for 3 h (LBNP+Saline) to maintain central blood volume unchanged, and 3) a control study without infusion or LBNP. During the Saline series, central venous pressure (CVP) and left atrial diameter (LAD) increased by 4.4 +/- 0.6 mmHg and 2.6 +/- 0.4 mm (P < 0.05), respectively, whereafter they declined toward preinfusion levels. During LBNP+Saline, CVP and LAD were unchanged. Plasma colloid osmotic pressure remained unchanged during control and showed identical decreases by 5 mmHg (P < 0.05) in the Saline and LBNP+Saline series. During the 3rd h of LBNP, renal sodium excretion (U(Na)V) peaked at 296 +/- 55 micromol/min vs. a higher value of 383 +/- 54 micromol/min (P < 0.05) during Saline. The increase in U(Na)V above that of control during the 3rd h of LBNP+Saline constituted 48% of that during Saline. Plasma renin activity and plasma aldosterone concentration showed similar patterns of decrease after saline infusion irrespective of LBNP, whereas plasma norepinephrine was elevated late in the LBNP period compared with during Saline and control (P < 0.05). It is concluded that the maintenance of a constant CVP and LAD reduces the natriuresis of acute saline loading by about one-half. Thus hemodilution in conjunction with suppression of renin and aldosterone release (independent of change in CVP and LAD) might account for the remaining natriuresis of infusion.

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

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.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Reflex control of the cutaneous circulation during passive body core heating in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Body Core ◽  
Doppler Techniques ◽  
The Impact

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

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