Effects of Pulmonary Blood Flow on Respiratory Mechanics: Measurements by the End-Inflation Occlusion Method in Healthy Rats After Acute Blood Volume Expansion

2010 ◽  
Vol 6 (3) ◽  
pp. 210-217
Author(s):  
Alessandro Rubini
1981 ◽  
Vol 60 (3) ◽  
pp. 283-293
Author(s):  
D. Querido ◽  
L. C. Isaacson

1. We have attempted to confirm the existence of a natriuretic hormone released in response to acute expansion of blood volume. 2. Isolated kidneys, perfused with whole blood at constant pressure, were incorporated within an extracorporeal circulation in recipient rats. In six control experiments urine flow rate, renal blood flow, glomerular filtration rate, filtration fraction, and the fractional excretion of filtered sodium and water were measured for periods of up to 120–140 min thereafter. The same variables were measured in a further 12 experiments in which, after 63 ± 11 min, the rats were volume expanded with equilibrated whole blood (15, 18 or 28 ml/kg body wt.). 3. On average the controls revealed no change in any of the variables measured; volume expansion was followed by increased renal blood flow and fractional excretion of filtered sodium and water, while the filtration fraction fell. 4. In both the control and volume-expansion experiments, there were 12 instances in which the fractional excretion of filtered sodium increased; in 10 of these, including those experiments in which the natriuresis was most marked, there was a closely correlated fall in filtration fraction. 5. In all the experiments changes in the fractional excretion of filtered sodium and water varied in parallel. 6. We conclude that volume expansion (a) changes the concentration of some circulating vasoactive substance(s) and (b) results in natriuresis and diuresis consequent upon a fall in filtration fraction.


Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3603-3610 ◽  
Author(s):  
Amy G. Tsai ◽  
Pedro Cabrales ◽  
Belur N. Manjula ◽  
Seetharama A. Acharya ◽  
Robert M. Winslow ◽  
...  

Abstract Cell-free hemoglobin's (CFH) high affinity for nitric oxide (NO) could limit CFH's use as an oxygen-carrying blood replacement fluid because it scavenges NO, causing vasoconstriction and hypertension. However, the extent to which perivascular NO levels change following intravascular administration of hemoglobin (Hb) with different molecular dimensions correlates with vasoconstrictive responses in the microcirculation is unknown. The study objective was to determine vasoconstrictive effects following bolus infusions of (1) αα cross-linked Hb; (2) polymerized bovine Hb; or (3) polyethylene glycol-decorated Hb (PEG-Hb), by measurements of in vivo microvessel diameter, blood flow, perivascular NO concentration, and systemic hemodynamic parameters. All CFHs caused reductions in perivascular NO levels, not correlated to microvascular responses. PEG-Hb (largest molecular volume) maintained blood flow, while the others caused vasoconstriction and reduced perfusion. All solutions increased mean arterial pressure due to vasoconstriction and blood volume expansion, except for PEG-Hb, which increased blood pressure due to blood volume expansion and maintenance of cardiac output. In conclusion, perivascular NO reduction is similar for all Hb solutions because NO binding affinities are similar; however, effects on vascular resistance are related to the type of molecular modification, molecular volume, and oxygen affinity.


1990 ◽  
Vol 22 (2) ◽  
pp. S102
Author(s):  
K. Norton ◽  
M. Delp ◽  
M. Jonas ◽  
C. Duan ◽  
D. Dengel ◽  
...  

1990 ◽  
Vol 69 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
M. T. Jones ◽  
C. Duan ◽  
D. R. Dengel ◽  
...  

To study the distribution of blood flow after blood volume expansion, seven miniature swine ran at high speed (17.6-20 km/h, estimated to require 115% of maximal O2 uptake) on a motor-driven treadmill on two occasions: once during normovolemia and once after an acute 15% blood volume expansion (homologous whole blood). O2 uptake, cardiac output, heart rate, mean arterial pressure, and distribution of blood flow (with radiolabeled microspheres) were measured at the same time during each of the exercise bouts. Maximal heart rate was identical between conditions (mean 266); mean arterial pressure was elevated during the hypovolemic exercise (149 +/- 5 vs. 137 +/- 6 mmHg). Although cardiac output was higher and arterial O2 saturation was maintained during the hypervolemic condition (10.5 +/- 0.7 vs. 9.3 +/- 0.6 l/min), O2 uptake was not different (1.74 +/- 0.08 vs. 1.74 +/- 0.09 l/min). Mean blood flows to cardiac (+12.9%), locomotory (+9.8%), and respiratory (+7.5%) muscles were all elevated during hypervolemic exercise, while visceral and brain blood flows were unchanged. Calculated resistances to flow in skeletal and cardiac muscle were not different between conditions. Under the experimental conditions of this study, O2 uptake in the miniature swine was limited at the level of the muscles during hypervolemic exercise. The results also indicate that neither intrinsic contractile properties of the heart nor coronary blood flow limits myocardial performance during normovolemic exercise, because both the pumping capacity of the heart and the coronary blood flow were elevated in the hypervolemic condition.


Respiration ◽  
2010 ◽  
Vol 79 (6) ◽  
pp. 497-505 ◽  
Author(s):  
A. Rubini ◽  
A. Gasperetti ◽  
V. Catena ◽  
D. Del Monte

1981 ◽  
Vol 241 (4) ◽  
pp. H571-H575 ◽  
Author(s):  
G. E. Billman ◽  
D. T. Dickey ◽  
K. K. Teoh ◽  
H. L. Stone

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.


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