Cardiac output, GFR, and renal excretion rates during maintained volume load in rats

1978 ◽  
Vol 235 (6) ◽  
pp. H670-H676 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Circulating Blood Volume ◽  
Reservoir Volume ◽  
Volume Load ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

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.

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.

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.

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.

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.

Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia

1992 ◽  
Vol 77 (2) ◽  
pp. 253-259 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Ted S. Keller ◽  
Glenn W. Kindt ◽  
David Archer
Keyword(s):  
Cardiac Output ◽  
Cerebral Ischemia ◽  
Blood Volume ◽  
Volume Expansion ◽  
Focal Cerebral Ischemia ◽  
Brain Regions ◽  
Ischemic Brain ◽  
Content Type ◽  
Blood Volume Expansion ◽  
Fine Print

✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001). The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.

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