scholarly journals Gastroduodenal resistance and neural mechanisms involved in saline flow decrease elicited by acute blood volume expansion in anesthetized rats

1997 ◽  
Vol 30 (10) ◽  
pp. 1257-1256 ◽  
Author(s):  
J.R.V. Graça ◽  
F. de-A.A. Gondim ◽  
D.I.M. Cavalcante ◽  
J. Xavier-Neto ◽  
E.L.M. Messias ◽  
...  
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Neural Mechanisms ◽  
Anesthetized Rats ◽  
Blood Volume Expansion

Control of right atrial pressure at constant cardiac output suppresses volume natriuresis in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 798-801 ◽  
Author(s):  
U. Ackermann ◽  
J. R. Rudolph
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Control Value ◽  
Volume Load ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Blood Volume Expansion

The blood volume of anesthetized rats was expanded acutely by 33% with donor blood while a caval snare was gradually tightened so that right atrial pressure (RAP) was prevented from rising (n = 6). In control experiments (n = 5) an aortic snare was used to hold mean arterial blood pressure near the values found in the experimental series. However, RAP was allowed to change freely and increased by 1.6 ± 0.4 mmHg (1 mmHg = 133.322 Pa) during volume expansion. When the two groups were compared, there were no significant differences between their mean arterial blood pressures (near 110 mmHg) or in their cardiac outputs (near 0.25 mL∙min−1∙g body weight−1). There were, however, significant differences between their renal responses to the volume load. When RAP was free to change, the rate of volume excretion [Formula: see text] increased to 30 ± 15 (SEM) μL∙min−1∙g kidney weight−1 (KW) from its control value of 3.49 ± 0.31 and the rate of sodium excretion [Formula: see text] increased to 3.59 ± 0.20 μequiv.∙min−1∙g KW−1 from its preinfusion value of 0.42 ± 0.10. When RAP was not allowed to increase during volume loading, [Formula: see text] and [Formula: see text] did not change from their respective preinfusion values (2.99 ± 0.46 μL∙min−1∙g KW−1 and 0.35 ± 0.10 μequiv.∙min−1∙g KW−1). The results imply that during acute blood volume expansion increased central vascular pressure is a prerequisite for the homeostasis of body water and salt.

Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

1981 ◽  
Vol 241 (4) ◽  
pp. H571-H575 ◽  
Author(s):  
G. E. Billman ◽  
D. T. Dickey ◽  
K. K. Teoh ◽  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Position ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Baroreflex Control ◽  
Beta Receptor ◽  
Blood Volume Expansion ◽  
Beta Receptor Blockade

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

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.

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