Effect of an acute increase in central blood volume on cerebral hemodynamics

2015 ◽  
Vol 309 (8) ◽  
pp. R902-R911 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Ai Hirasawa ◽  
Peter B. Raven ◽  
Thomas Rebuffat ◽  
Pierre Denise ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Parabolic Flight ◽  
Central Blood Volume ◽  
Arterial Pulse ◽  
Vascular Conductance ◽  
Systemic Hemodynamic ◽  
Arterial Pulse Pressure ◽  
Acute Increase

Systemic blood distribution is an important factor involved in regulating cerebral blood flow (CBF). However, the effect of an acute change in central blood volume (CBV) on CBF regulation remains unclear. To address our question, we sought to examine the CBF and systemic hemodynamic responses to microgravity during parabolic flight. Twelve healthy subjects were seated upright and exposed to microgravity during parabolic flight. During the brief periods of microgravity, mean arterial pressure was decreased (−26 ± 1%, P < 0.001), despite an increase in cardiac output (+21 ± 6%, P < 0.001). During microgravity, central arterial pulse pressure and estimated carotid sinus pressure increased rapidly. In addition, this increase in central arterial pulse pressure was associated with an arterial baroreflex-mediated decrease in heart rate ( r = −0.888, P < 0.0001) and an increase in total vascular conductance ( r = 0.711, P < 0.001). The middle cerebral artery mean blood velocity (MCA Vmean) remained unchanged throughout parabolic flight ( P = 0.30). During microgravity the contribution of cardiac output to MCA Vmean was gradually reduced ( P < 0.05), and its contribution was negatively correlated with an increase in total vascular conductance ( r = −0.683, P < 0.0001). These findings suggest that the acute loading of the arterial and cardiopulmonary baroreceptors by increases in CBV during microgravity results in acute and marked systemic vasodilation. Furthermore, we conclude that this marked systemic vasodilation decreases the contribution of cardiac output to CBF. These findings suggest that the arterial and cardiopulmonary baroreflex-mediated peripheral vasodilation along with dynamic cerebral autoregulation counteracts a cerebral overperfusion, which otherwise would occur during acute increases in CBV.

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.

scholarly journals Relationship between Stroke Volume and Pulse Pressure during Blood Volume Perturbation: A Mathematical Analysis

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Ramin Bighamian ◽  
Jin-Oh Hahn
Keyword(s):  
Stroke Volume ◽  
Blood Volume ◽  
Fluid Therapy ◽  
Pulse Pressure ◽  
Mathematical Analysis ◽  
Left Ventricular ◽  
Experimental Investigations ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
Relative Change

Arterial pulse pressure has been widely used as surrogate of stroke volume, for example, in the guidance of fluid therapy. However, recent experimental investigations suggest that arterial pulse pressure is not linearly proportional to stroke volume. However, mechanisms underlying the relation between the two have not been clearly understood. The goal of this study was to elucidate how arterial pulse pressure and stroke volume respond to a perturbation in the left ventricular blood volume based on a systematic mathematical analysis. Both our mathematical analysis and experimental data showed that the relative change in arterial pulse pressure due to a left ventricular blood volume perturbation was consistently smaller than the corresponding relative change in stroke volume, due to the nonlinear left ventricular pressure-volume relation during diastole that reduces the sensitivity of arterial pulse pressure to perturbations in the left ventricular blood volume. Therefore, arterial pulse pressure must be used with care when used as surrogate of stroke volume in guiding fluid therapy.

Determination of central blood volume. Comparison of Stewart-Hamilton method with direct measurements in dogs

1959 ◽  
Vol 196 (3) ◽  
pp. 499-501 ◽  
Author(s):  
Robert C. Schlant ◽  
Paul Novack ◽  
William L. Kraus ◽  
Charles B. Moore ◽  
Florence W. Haynes ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Transit Time ◽  
Mean Transit Time ◽  
Total Radioactivity ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Central Blood Volume ◽  
Volume Comparison ◽  
Direct Measurements

Central blood volume (cardiac output times mean transit time) from right atrium to ascending aorta was determined by the indicator-dilution method in 22 open-chested dogs which had previously had their red blood cells tagged with Cr51. The actual amount of blood in the heart and lungs was calculated from the total radioactivity in the blended homogenate of these organs. The two measurements of central blood volume correlated well ( r = +.88), the indicator-dilution volumes averaging 12% greater. The discrepancy between measurements is probably related to the pulmonary circuit having a lower hematocrit than the large vessels. The results substantiate the use of the Stewart-Hamilton formula (cardiac output times mean transit time) to measure central blood volume.

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs

1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Ang Ii ◽  
Central Blood Volume ◽  
Venous Compliance ◽  
Induced Hypertension

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure

1993 ◽  
Vol 264 (5) ◽  
pp. R1024-R1030 ◽  
Author(s):  
P. Norsk ◽  
P. Ellegaard ◽  
R. Videbaek ◽  
C. Stadeager ◽  
F. Jessen ◽  
...  
Keyword(s):  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Pulse ◽  
Vasopressin Release ◽  
Arterial Pulse Pressure ◽  
Arterial Plasma

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

scholarly journals SP284ARTERIAL STIFFNESS CALCULATED FROM PERIPHERAL ARTERIAL PULSE PRESSURE IS INDEPENDENTLY ASSOCIATED WITH ALL-CAUSE MORTALITY IN THE GENERAL POPULATION

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i183-i183
Author(s):  
Maarten A de Jong ◽  
Arie M van Roon ◽  
Jens T Bakker ◽  
Wernard Kersten ◽  
Pieter W. Kamphuisen ◽  
...  
Keyword(s):  
General Population ◽  
Pulse Pressure ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
All Cause Mortality ◽  
Peripheral Arterial
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