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Biomedical subjects

U Ackermann

Publications and source records attributed to U Ackermann.

At least 55 records · Page 3Linked to original sources
PubMed1984

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

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 X min-1 X 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 (V) increased to 30 +/- 15 (SEM) microL X min-1 X g kidney weight-1 (KW) from its control value of 3.49 +/- 0.31 and the rate of sodium excretion (UNaV) increased to 3.59 +/- 0.20 muequiv X min-1 X g KW-1 from its preinfusion value of 0.42 +/- 0.10. When RAP was not allowed to increase during volume loading, V and UNaV did not change from their respective preinfusion values (2.99 +/- 0.46 microL X min-1 X g KW-1 and 0.35 +/- 0.10 muequiv X min-1 X 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.

Anesthesia↗
PubMed1984

Cardiovascular effects of atrial extracts in anesthetized rats.

Tissue extracts derived from atria or ventricles of Sprague-Dawley rats were injected into Inactin-anesthetized assay rats. Compared with ventricular extracts, atrial extracts produced a 20 mmHg (1 mmHg = 133.322 Pa) fall in mean arterial blood pressure. This fall resulted from failure to increase cardiac output in compensation for peripheral vasodilation. Two factors were responsible: depression of heart rate (by 25 beats/min) and failure to increase cardiac performance. The time patterns and magnitudes of changes in cardiovascular parameters after cardiac extracts were not changed by prior atropinization. However, assay rats that were vagotomized showed no cardiac slowing after atrial extract and showed a significantly smaller decrease in mean arterial blood pressure than did sham-vagotomized or intact rats. Another group of assay rats was vagotomized as well as carotid-sinus-denervated before extract injection. In these rats the degree of hypotension caused by atrial extract was significantly greater than that observed after vagotomy alone and was not significantly different from that observed in rats with intact innervation. The results suggest that the hypotension that is caused by atrial extract, but not by ventricular extracts, results in part from the reflex effects of direct stimulation of chemosensitive cardiopulmonary receptors with vagal afferents and partly from the reflex effects of baroreceptor unloading. Ventricular extract had no hypotensive effect in any group of assay rats.

Animals↗
PubMed1984

Synthesis and renal activity of rat atrial granules depend on extracellular volume.

Extracellular fluid volume (by 22Na) and extent of 4-h [3H]fucose incorporation into atrial-specific granules were measured in deoxycorticosterone acetate (DOCA)/salt-loaded or Na-deficient rats. The natriuretic potency of extracts from their atria was also measured in assay rats. DOCA/salt-treated animals had a significantly greater extracellular volume, a significantly greater degree of fucose uptake, and a significantly more potent diuretic and natriuretic effect than did Na-deficient rats. These observations, together with the known decrease in atrial granularity with DOCA treatment, suggest that a chronic increase in extracellular fluid volume is associated with increased synthesis and metabolism of atrial natriuretic factor. They also confirm the finding reported by others that granularity and natriuretic potency are not always directly related. It may be that visible granules represent a peptide storage form that requires further processing to become natriuretic.

Animals↗
PubMed1980

Control of renal function in isovolemic hemodilution or in vagotomized, infused rats.

In male Sprague-Dawley rats cardiac output (CO) was increased 0.16 ml/min x g body weight and inulin clearance was increased 2.2 ml/min x g kidney weight either by isovolemic hemodilution with 6% albumin solution or by isohemic expansion to 133% of control blood volume. Despite similar changes in CO and glomerular filtration (GFR), hemodilution caused a much smaller rise in renal excretion at a much later time than did volume expansion. Therefore, in addition to simultaneous changes in CO and GFR and afferent factor indicating a state of expanded extracellular fluid volume was required for normal diuresis and natriuresis. This might have been mean central venous pressure (CVP). In further experiments, volume expansion in vagotomized or non-vagotomized rats led to nearly identical changes in water-, sodium- and potassium excretion in both groups. The only other measured parameter that showed identical behaviour in the two groups was CVP. It was concluded that CVP is an important contributor to body fluid control mechanisms even after vagotomy.

Animals↗
PubMed1980

Renal blood flow distribution measured by microspheres during isovolemic hematocrit alteration in rats.

The distribution of 15-micron microspheres was measured in rat kidneys before and after the animals had undergone either isovolemic hematocrit increase or isovolemic hematocrit decrease. Raising the systemic arterial hematocrit from 46 +/- 1% (mean +/- SEM) to 59 +/- 1% caused a significant decrease in the rate of urinary sodium and potassium excretion (UNaV, UKV), but not significant changes in total renal blood flow (RBF), filtration fraction (FF), outer cortical flow, inner cortical flow, or rate of urinary volume excretion (V). Fractional sodium excretion was also unchanged suggesting that the decreased UNAV was the result of a decreased glomerular filtration rate (GFR). The measured decrease in GFR was not statistically significant. Lowering the systemic hematocrit from 45 +/- 1% to 33 +/- 1% caused a significant fall in FF as well as significant increases in the rate of urine volume excretion (V), UNaV, UKV, and GRF. There was a significant increase in RBF but again no change in the flow distribution between inner and outer cortex. The findings show that hematocrit alterations alone do not immediately lead to a redistribution of blood flow between inner and outer cortex of the rat kidney.

Animals↗
PubMed1980

Regional blood flows and cardiac output distribution in rats during acute anemia or polycythemia.

Radioactively labelled microspheres (15 micron diameter) were used to measure cardiac output (CO) distribution and blood flows in spleen, kidneys, and skeletal muscle before and after normovolemic anemia or polycythemia in anesthetized rats. Hematocrits were changed from 45 to 33% or from 45 to 59% by an exchange transfusion of homologous plasma or packed cells. Anemia was accompanied by a 39% increase in CO while polycythemia showed a 25% decrease. Following hemodilution the spleen as well as skeletal muscle received greater than normal fractions of CO and in each the flow increase was greater than expected from the fall in viscosity. The renal fraction of CO was unchanged. Following hemoconcentration "greater-than-normal" fractions of CO were distributed towards spleen and kidney. In these tissues the changes in flow were significantly greater than the change in resistance due to viscosity. Skeletal muscle flow changes appeared to have been due mostly to increased viscosity. These observations imply that during acute, isovolemic changes in hematocrit, the flow changes of individual vascular beds cannot be explained by viscosity changes alone but the importance of nervous control or of local metabolic factors remains to be investigated.

Anemia↗
PubMed1978

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

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.

Animals↗
PubMed1978

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

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.

Animals↗
PubMed1978

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

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.

Animals↗
PubMed1977

Changes in interstitial pressure during acute interstitial volume depletion in normally hydrated rats.

Interstitial fluid pressure was measured in normally hydrated rats during acute interstitial volume depletion by intravenous hyperoncotic bovine serum albumin infusion. Body fluid volumes, systemic arterial and venous pressure and selected blood and urine variables were also measured. The infusion increased plasma volume twice as much as do iso-oncotic infusions which cause comparable increases in mean central venous pressure. The kidneys responded with a diuresis and natriuresis closely resembling those which follow iso-oncotic infusion in normally hydrated rats. At the end of the elevated renal response plasma volume and plasma protein concentration were not restored to pre-infusion values; total interstitial fluid volume was decreased to one half its control value. Interstitial fluid pressure decreased linearly with volume so that effective interstitial compliance was constant at 0.0717 ml/mm Hg per gram dry tissue weight (1.79 ml/mm Hg per 100 g BW). This was not significantly different from the value 0.0704 previously found in normally hydrated rats but very significantly higher than that in dehydrated rats with comparable interstitial depletion. It is concluded that interstitial compliance is normal over a wide range of interstitial fluid volume in normally hydrated rats but that it can be altered in states of chronic body water depletion.

Animals↗
PubMed1976

Changes in interstitial pressure during and after blood volume expansion in rats.

Interstitial fluid pressure was measured via a chronically implanted capsule before, during and after acute isotonic, iso-oncotic blood volume expansion in normal or in 48-h dehydrated rats. At the same time, the patterns of body fluid distribution, of selected renal responses and of mean arterial and mean central venous pressure responses were studied. Dry tissue weight (DTW) was subsequently determined by freeze drying of the shaved carcass. Dehydration decreased plasma volume and interstitial fluid volume significantly below normal values. The initial intracapsular pressure in dehydrated animals (-3.7 +/- 0.6 mm Hg) was not significantly different from that in normal rats (-2.5 +/- 0.5), but dehydrated rats showed initially a very significantly lower effective interstitial compliance (0.0005 ml/mm Hg per gram DTW) than did the normal group (0.0704). In the course of the renal response to the volume load, effective interstitial compliance increased to 0.0350 in dehydrated rats but showed no change in normal rats. Neither group completely corrected its elevated blood volume; both returned their central venous pressures to pre-infusion levels; both decreased their interstitial fluid volumes below pre-infusion levels and both decreased their intracapsular fluid pressures 1 mm Hg below the level prevailing in non-infused animals at that time. It is concluded that a reduction in interstitial hydrostatic pressure can be a functionally important influence in the apparent control of central venous pressure following acute blood volume expansion.

Animals↗
PubMed1975

On the role of the interstitial volume in the response of the rat to blood volume expansion.

Patterns of body fluid distribution and selected cardiovascular and renal responses were studied following vascular expansion in normal rats and in rats with altered interstitial fluid volume produced by dehydration, prehydration or hyperoncotic albumin infusion. In all four groups the patterns of the renal excretory response and the accompanying change in central venous pressure (CVP) were closely parallel and the disturbance in CVP was finally corrected in the presence of a considerable residual vascular expansion. During the diuresis and saluresis following iso-oncotic vascular expansion in prehydrated and dehydrated rats, both groups removed fluid chiefly from the interstitium; this fluid removal was attributable mainly to urinary excretion in prehydrated rats but mainly to redistribution into the cellsin dehydrated rats. In the latter series, preferential renal excretion of sodium over water was observed. Hyperoncotic vascular expansion led to a peak renal excretory response only 70% of that following iso-oncotic expansion. The excreted volume was accounted for by a similar depletion of interstitial fluid after the iso-oncotic load. These findings are consistent with the hypothesis that the renal response to volume expansion regulates some parameter which is more closely related to the mean central venous pressure than to the vascular volume. This regulation was associated with incomplete correction of the vascular expansion and absolute decrease in interstitial fluid volume compared to the initial size of that compartment. This provides support for a functionally important influence of the interstitial volume on venous compliance.

Animals↗
PubMed1975

An approach to the measurement of body fluid compartment volumes in non-steady conditions in the rat.

A method has been developed by which body fluid volume changes can be assessed frequently after only one initial injection of the appropriate radioactive tracers. This method is based on the assumptions that, 1. following their intravenous injection, the temporal behaviour of tritiated water or radio-sodium can be adequately modelled by the kinetic behaviour of an open, interconnected two-compartment system; 2. known amounts of tracer are added to or irreversibly removed from the system only via the first compartment. In the measurement of body fluid volume changes in rats after isotonic blood volume expansion, the rapid urinary tracer excretion was treated as a series of negative tracer "injections" made instantaneously into the first tracer compartment at the mid point of each short urine collection period. The effect of these "injections" on the first compartment was regarded as diminishing with time in accordance with the steady state rate constants. The vaolues for non steady state changes in total body water volume and functional extracellular fluid volume obtained by such a mathematical treatment, agreed closely with directly measured changes where such direct comparisons could be made.

Animals↗
PubMed1975

On the regulation of the renal response blood volume expansion by vascular parameters in the rat.

The dynamic patterns of body fluid volume distribution, of cardiovascular variables and of renal water, sodium and potassium excretion were studied in the anaesthetized rat following acute, iso-oncotic blood volume expansion. The increased renal excretion following expansion was soon reversed and its pattern to termination was not correlated with changes in pulse and mean arterial pressure, in plasma electrolyte concentration or in haematocrit. At the end of the renal response the change in extracellular fluid volume was not usually corrected, the blood volume was always well above its control value and the interstitial fluid was below its control value. In all cases the temporal pattern and the termination of the renal response corresponded closely with the temporal pattern and the return to the control value of the central venous mean and pulse pressure. The findings of thse experiments are not consistent with the view that any of the measured body fluid volumes directly and always determine renal excretion. It is proposed that in response to an acute blood volume expansion an animal may initially regulate neither its blood volume nor its extracellular fluid volume but rather a factor which is reflected in or related to the central venous pressure.

Animals↗