The Effect of Plasma from Blood Volume Expanded Dogs on Sodium, Potassium and Pah Transport of Renal Tubule Fragments

1970 ◽  
Vol 38 (6) ◽  
pp. 617-627 ◽  
Author(s):  
E. M. Clarkson ◽  
L. B. Talner ◽  
H. E. de Wardener
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Renal Tubule ◽  
Sodium Potassium ◽  
Transport Studies ◽  
Blood Volume Expansion ◽  
Before And After ◽  
Control Plasma ◽  
Sodium And Potassium

1. Sodium, potassium and para-amino hippurate (PAH) transport was studied in renal tubule fragments incubated in vitro in plasma taken from dogs before and after their blood volume was expanded with blood with which the dog was in equilibrium. The individuals who carried out the cell transport studies did not know the identity of the plasma samples. 2. Tubule fragments were less able to maintain a gradient of sodium and potassium, or to accumulate PAH when incubated in plasma obtained after blood volume expansion than when they were incubated in control plasma. 3. It is concluded that expansion of the blood volume causes the dog to change the concentration of some unknown circulating substance which influences sodium, potassium and PAH transport in separated tubule fragments. 4. It is proposed that this substance is partly responsible for the rise in urinary excretion of sodium that accompanies blood volume expansion in the intact animal.

Apparent escape rate of RIHSA and 51Cr-labeled erythrocytes from the blood of volume-expanded rats

1978 ◽  
Vol 234 (5) ◽  
pp. F386-F392
Author(s):  
U. Ackermann
Keyword(s):  
Blood Volume ◽  
Rate Constant ◽  
Volume Expansion ◽  
Whole Body ◽  
Bovine Albumin ◽  
Blood Volume Expansion ◽  
Average Slope ◽  
Before And After ◽  
Nonsteady State ◽  
Whole Body Hematocrit

The disappearance rate constant of radioiodinated human serum albumin (RIHSA) and 51Cr-tagged erythrocytes was measured in rats before and after intravenous, isoncotic blood volume expansion (6% bovine albumin; 75 or 33% of blood volume). Before volume expansion the average slope of the semilogarithmically plotted plasma RIHSA activity was -2.068 X 10(-3) +/- 0.146 X 10(-3) (SE) min-1. The slope was not significantly changed when tested by subsequent tracer injections which were made immediately after and 1 h after volume expansion. Preinfusion plasma volume (PV) was constant, but total erythrocyte volume (RCV) increased at a significant rate from 0.0253 +/- 0.0030 to 0.0300 +/- 0.0038 ml/g body wt over the 2-h period. PV was elevated and RCV was unchanged by the infusion, but both decreased significantly thereafter. The observed erythrocyte loss could not be accounted for by sampling or bleeding. Arterial hematocrit remained constant while RCV and PV were decreasing, and it was identical to whole-body hematocrit throughout. It was concluded that 1) isoncotic albumin expansion did not change the rate constant of transcapillary albumin loss; 2) nonsteady state PV could be calculated from a single preinfusion RIHSA dose; and 3) sequestration of blood may be a part of the rat's response to volume expansion.

Kidney function in ANF-transgenic mice: effect of blood volume expansion

1991 ◽  
Vol 260 (1) ◽  
pp. R1-R5 ◽  
Author(s):  
L. J. Field ◽  
A. T. Veress ◽  
M. E. Steinhelper ◽  
K. Cochrane ◽  
H. Sonnenberg
Keyword(s):  
Transgenic Mice ◽  
Kidney Function ◽  
Blood Volume ◽  
Volume Expansion ◽  
Fusion Gene ◽  
Transgenic Animals ◽  
Renal Perfusion ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Before And After

Transgenic mice, created from inbred C3HeB/FeJ embryos, were used to overexpress selectively in the liver a fusion gene comprising mouse transthyretin (TTR) regulatory and atrial natriuretic factor (ANF) structural sequences. Animals were anesthetized, and kidney function was studied before and after blood volume expansion. Baseline urine volumes and electrolyte excretions were not significantly different from those of non-transgenic littermates, despite a markedly lower arterial blood pressure in the experimental group. A slightly lower glomerular filtration rate (GFR) in transgenics was not different statistically. Plasma ANF levels measured by radioimmunoassay were approximately 10-fold higher in the transgenic animals, compared with their nontransgenic siblings. After acute blood volume expansion, the diuretic, natriuretic, kaliuretic, and chloruretic responses were markedly enhanced in the transgenic group. Arterial pressure was increased as a result of hypervolemia, although it remained relatively depressed relative to the controls. GFR again was not different. We conclude that transgenic mice overexpressing ANF can maintain normal excretion of salt and water, possibly via ANF-induced reduction of renal perfusion pressure. After acute blood volume expansion, an increase in pressure may allow full renal expression of the chronically elevated ANF levels.

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.

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

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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