Rat venular pressure-diameter relationships are regulated by sympathetic activity

1990 ◽  
Vol 259 (3) ◽  
pp. H674-H680 ◽  
Author(s):  
A. A. Shoukas ◽  
H. G. Bohlen
Keyword(s):  
Blood Volume ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Nervous System Activity ◽  
Blood Volume Expansion ◽  
Capacitance Characteristics ◽  
Sympathetic Nervous ◽  
Relationship Of ◽  
The Relationship

The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.

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.

Baroreflex regulation of hindquarter vascular resistance during acute blood volume expansion

1984 ◽  
Vol 246 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
G. B. Guo ◽  
D. R. Richardson
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Time Course ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Baroreflex Control ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors ◽  
Cardiopulmonary Baroreceptors

The baroreflex control of hindquarter vascular resistance in response to a 30% blood volume expansion (BVE) was examined in constant-flow perfused hindlimbs of chloralose-urethan-anesthetized rats. Volume expansion initially increased both systemic arterial pressure (SAP) and central venous pressure (CVP) while decreasing hindquarter vascular resistance. After these initial changes, there was a parallel return of hindquarter-vascular resistance and CVP to pre-expansion levels, suggesting that cardiopulmonary afferents play a major role in the vascular resistance adjustments to volume expansion. This notion was supported in a separate set of experiments in which CVP was elevated selectively while SAP was held constant. This manipulation elicited a decrease in hindquarter vascular resistance, which was significantly attenuated following vagal cardiopulmonary denervation. The return of hindquarter vascular resistance following BVE also occurred in the presence of elevated SAP in rats with vagotomy and aortic nerve denervation, i.e., only the carotid sinus baroreflexes intact, but the time course was much faster compared with preparations with cardiopulmonary receptors intact. No response of hindquarter vascular resistance to BVE was observed in rats with both sinoaortic and cardiopulmonary baroreceptors denervated. These findings suggest that the return of hindquarter vascular resistance following BVE involves a gradual increase in sympathetic outflow to the hindquarters resulting from both a decrease in cardiopulmonary afferent activity and a rapid adaptation of arterial baroreflexes.

Quantitative Evaluation of the Circulatory Adjustment of Splenectomized Dogs to Hemorrhage

1958 ◽  
Vol 193 (3) ◽  
pp. 605-614 ◽  
Author(s):  
Shu Chien
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Sympathetic Activity ◽  
Volume Reduction ◽  
Fluid Replacement ◽  
Maximum Heart Rate ◽  
Equal Importance ◽  
Sympathetic Nervous ◽  
The Relationship

Controlled, single hemorrhages were carried out in splenectomized dogs (5–49% of blood volume) and sympathectomized-splenectomized dogs (5–32% of blood volume). A linear relationship exists between the degree of hemodilution and the amount of hemorrhage in both groups. Sympathetic activity aids in the fluid replacement after hemorrhage. In the sympathectomized-splenectomized dogs, the relationship between arterial pressure and blood volume reduction seems to be nonlinear. Arterial pressure of the splenectomized dogs does not decrease until blood volume reduction is more than 10%. Thereafter it decreases linearly with increasing volume reduction which is still compatible with life. In hemorrhages between 10 and 40% of blood volume, the roles played by sympathetic activity and hemodilution in the maintenance of arterial pressure are of about equal importance. The increase in heart rate after hemorrhage has S-shaped relationship to both blood volume reduction and arterial pressure decrease in dogs with or without sympathetic nervous system. The maximum heart rate displayed by sympathectomized dogs after hemorrhage (about 120 beats/min.) is much less than that of the dogs with sympathetic system intact (about 215 beats/min.). The activation of sympathetic activity is not fully achieved immediately after hemorrhage.

Water and Sodium Excretion after Blood Volume Expansion under Conditions of Constant Arterial, Venous and Plasma Oncotic Pressures and Constant Haematocrit

1972 ◽  
Vol 42 (6) ◽  
pp. 701-709 ◽  
Author(s):  
B. Lichardus ◽  
A. Nizet
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Specific Factor ◽  
Experimental Conditions ◽  
Natriuretic Hormone ◽  
Arterial Perfusion ◽  
Homologous Blood Transfusion ◽  
Blood Volume Expansion

1. The diuretic and natriuretic responses occurring during expansion of blood volume by homologous blood transfusion were studied in homologous kidneys transplanted to the neck of hydropenic dogs that had previously been given deoxycorticosterone acetate and antidiuretic hormone. The experimental conditions ensured constant arterial perfusion pressure, venous pressure, osmotic pressure, haematocrit and plasma oncotic pressure. 2. Moderate but significant increases in urine output, renal sodium excretion, osmotic clearance and tubular sodium rejection fraction were observed; there were no significant changes in glomerular filtration rate, renal blood flow, postglomerular haematocrit and postglomerular plasma protein concentration 20 and 40 min after the end of blood infusion. 3. As the non-hormonal factors known to modulate sodium excretion underwent no significant change, the results are compatible with the proposition that a specific factor (‘natriuretic hormone’) plays a role in the mechanism of natriuresis after blood volume expansion.

Increased ANF secretion after volume expansion is preserved in rats with heart failure

1988 ◽  
Vol 254 (2) ◽  
pp. R185-R191 ◽  
Author(s):  
Y. W. Chien ◽  
R. W. Barbee ◽  
A. A. MacPhee ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Blood Volume ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Blood Volume Expansion

To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P less than 0.01), cardiac index (-27%, P less than 0.001), renal blood flow (-35%, P less than 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P less than 0.01), and increases in central venous pressure (+1.7 mmHg, P less than 0.01), left ventricular end-diastolic pressure (+10 mmHg, P less than 0.001), total peripheral resistance (+28%, P less than 0.01), and plasma ANF level (752 +/- 109 vs. 244 +/- 33 pg/ml, P less than 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricle pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 +/- 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.

Plasma release of atrial natriuretic peptide in response to blood volume expansion

1986 ◽  
Vol 109 (1) ◽  
pp. 9-13 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Christofides ◽  
S. R. Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Colloidal Solution ◽  
Venous Pressure ◽  
Molecular Size ◽  
Rat Plasma ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

ABSTRACT The response of plasma atrial natriuretic peptide (ANP) concentration to acute intravascular volume expansion was measured in ten male Wistar rats. An infusion of 3 ml polygelene colloidal solution at 37 °C over 45 s produced peak venous pressure rises of 1·5cm water. A highly significant (P<0·001) rise of immunoreactive plasma ANP from 24·4 ± 2·2 (mean ± s.e.m.) pmol/l to a peak of 70·0±10·5 pmol/l occurred within 2·5 min. Plasma ANP concentrations had virtually returned to basal levels (32·7 ± 2·7 pmol/l) 30 min after this acute volume load. A further infusion of 10 ml polygelene colloidal solution in 2 min produced peak venous pressure rises of 10 cm water and caused a dramatic and significant (P< 0·001) increase of plasma ANP concentration to a peak of 534·8 ± 38·5 pmol/l, occurring 7·5 min after infusion. The plasma ANP concentration had fallen but remained above basal levels 30 min later (137·2 ± 26·4 pmol/l). Similar results were obtained using an identical protocol but with whole rat blood instead of polygelene solution as the volume-expanding agent. Gel column chromatography suggested that the majority of the immunoreactive ANP in rat plasma was of similar molecular size to rat α-ANP(1–28). These results support the hypothesis that blood volume expansion is a potent stimulus for the release of ANP into plasma. J. Endocr. (1986) 109, 9–13

Renal venous pressure and volume natriuresis in the rat

1984 ◽  
Vol 62 (1) ◽  
pp. 80-83 ◽  
Author(s):  
John R. Rudolph ◽  
Uwe Ackermann
Keyword(s):  
Blood Volume ◽  
Renal Vein ◽  
Volume Expansion ◽  
Renal Excretion ◽  
Left Kidney ◽  
Venous Pressure ◽  
Blood Volume Expansion ◽  
Excretion Rates ◽  
The Right ◽  
Pressure Changes

Anesthetized rats were surgically prepared so that left renal venous pressure could be maintained at its normal level (near 1 mmHg) (1 mmHg = 133.322 Pa) while right renal venous pressure was free to change in response to acute isoncotic blood volume expansion (n = 10). The purpose of the study was to test whether the renal venous pressure changes normally accompanying a 33% blood volume expansion have an effect on inulin clearance (CIn) and on the rates of excretion of water [Formula: see text] or sodium [Formula: see text] by the kidneys. In 10 control rats blood volume was not expanded. The results showed that the volume expansion used resulted in a peak pressure of 5.3 ± 0.5 (SEM) mmHg in the right renal vein. Both kidneys showed significant increases in CIn, [Formula: see text], and [Formula: see text] over their respective preexpansion values. However, there were no significant differences between these parameters measured in the right or in the left kidney even though the differences between the two renal venous pressures were highly significant during the infusion and for the next 20 min. In a further six rats, a caval snare was placed superior to the right renal vein so that both renal venous pressures could be held at normal during blood volume expansion. The ensuing diuresis and natriuresis were not different from those observed in the preceding group. It is concluded that changes in renal venous pressure, of the magnitude associated with volume expansion, have no significant effect on renal excretion rates.

Effects of increased splenic arterial flow and venous pressure on splenic red cell accumulation

1990 ◽  
Vol 258 (3) ◽  
pp. H669-H678
Author(s):  
J. Thorvaldson ◽  
O. Stokland ◽  
A. Ilebekk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Red Cells ◽  
Arterial Flow ◽  
Red Cell ◽  
Blood Volume Expansion ◽  
Cell Accumulation ◽  
Anesthetized Dogs

The importance of increments in splenic venous pressure (SVP) and splenic arterial flow (SAF) for splenic red cell accumulation was estimated in 14 anesthetized dogs with the spleen in situ by arterial and splenic venous hematocrit measurements and continuous ultrasonic recording of splenic diameter (SD). A 10-mmHg increase in SVP by 4 min of splenic venous constriction reduced SAF by 32 +/- 5%, increased SD by 5.1 +/- 0.8%, and transiently reduced splenic venous hematocrit, measured every 10 s, from 35.4 +/- 1.4 to a minimum of 29.2 +/- 1.8%. A 10-mmHg rise in SVP by 4 min of saline infusion increased SAF by 178 +/- 25% and SD by 16.1 +/- 3.0%, and splenic venous hematocrit declined more rapidly and to a lower value than arterial hematocrit. Blood volume expansion with saline or blood at constant, 10-mmHg elevated SVP confirmed that splenic red cell accumulation was greater during blood volume expansion than during splenic venous constriction. We conclude that the spleen accumulates red cells when SVP is raised. At constant, elevated SVP splenic red cell accumulation is flow dependent.

Cardiac output and renal excretion rates during acute blood volume expansion in rats

1978 ◽  
Vol 234 (1) ◽  
pp. H21-H27 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Volume Expansion ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Plasma Protein Concentration ◽  
Renal Response ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

Selected central vascular parameters and renal excretion rates were monitored in anesthetized rats after acute, isohemic blood volume expansion by 33 percent. The infusate was an equilibrated mixture of animals' own blood and isotonic, isoncotic (6 percent) bovine albumin. Expansion increased mean arterial pressure by 35 percent, mean central venous pressure (CVP) by 850 percent, cardiac output (CO) by 56 percent, hematocrit (Hct) by 25 percent, plasma protein concentration (Ppr) by 25 percent, renal excretion rates of volume by 4,400 percent, of sodium by 2,800 percent, and of potassium by 360 percent of the respective preinfusion value. Hct and Ppr measurements suggested that 15 min after the end of the infusion, only 33 percent of infused volume remained within the circulation and that there was little further change in this during the remainder of the experiment. At the end of the elevated renal response, CVP and CO alone had returned to control values. Renal excretion rates were highly correlated with CO, but they were delayed by 2-5 min with respect to it. The results suggest that the renal response to acute volume expansion does not primarily control blood volume. Cardiac output may be the controlled variable in the response.

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