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H Tost

Publications and source records attributed to H Tost.

At least 19 recordsLinked to original sources
PubMed1991

Investigations on the circulation of anesthetized dogs.

In the present experiments arterial blood pressure, cardiac output, heart rate, oxygen consumption, AVO2 difference values and their changes were investigated in 64 anesthetized dogs in four periods for altogether 60 min. Blood flows of the renal, commune carotid and femoral arteries were measured in parallel and the changes were recorded throughout the 60 min of the experimental period. Urine was collected separately from both kidneys, in order to determine whether the measurement of the blood flow of the renal artery disturbed renal functions. Total peripheral vascular resistance and the vascular resistance of the territories of the commune carotid and femoral arteries were calculated from the parameters measured. In the present experiments the equation of the regression line between cardiac output and body weight was y = 0.102x + 0.9411. The equation of the regression line between cardiac output an body surface proved to be y = 2.996x + 0.653. The relationship between total oxygen consumption and body weight could be characterized by the y = 5.815x + 24.227 equation. Our data were in accordance with data of the Biology Data Book obtained in dogs anesthetized by pentobarbital. Our present data can be found but partially in the Biology Data Book, so the results obtained in the present study may serve as basis of future comparisons. In this work proper care was taken to maintain the same conditions and, thus ruling out possible artefacts. The experiments were carried out on mongrel dogs of different sexes; nevertheless, the animals were attempted to be kept under the same conditions for the 14 days preceding the experiments.

Anesthesia↗
PubMed1990

The effect of lidocain on the renal function.

The evidence supporting a role for direct neurogenic control of renal function was investigated in twenty anaesthetized dogs. Unilateral renal sympathectomy was induced by 0.5 mg/kg/min of lidocain infusion into the left renal artery and the kidney function changes were compared to those observed in the right non infused kidney. The renal parameters were similar in the kidneys during the control periods. 0.5 mg/kg/min of lidocain infusion into the left renal artery resulted in significant reductions of the RBF, GFR, urine and sodium excretion in the left kidney. The intrarenal lidocain infusion induced a small decrease of the arterial blood pressure but this can not explain the changes observed in the left kidney. The modifications of the right kidney function during lidocain infusion were significantly less than those observed in the left kidney. Comparing the measured RBF and the renal blood flow calculated by the CPAH in the left kidney during the lidocain infusion, we have found a marked difference, when the decrease of the calculated RBF was greater. We believe that effects of pharmacological denervation can be best explained by the intrarenal hemodinamically mediated changes. The sympathectomy produces a considerable vasoconstriction in the renal cortical vascular bed, subsequently it decreases the RBF, GFR renal sodium and water excretion. But the lidocain blocks the sympathetic nerves influencing the renal medullary vessels and the renal medullary blood flow increases. These observations are not consistent with the notion that renal nerves are at least partially responsible for the natriuresis accompanying salt loading.

Animals↗
PubMed1989

The effect of Ringer solution induced extracellular volume expansion on kidney function.

The present study quantitated the effects of extracellular volume expansion on sodium and water excretion in 118 anesthetized dogs. The animals received a priming injection of 10 ml kg-1 Ringer solution i.v. which was followed by a constant Ringer solution infusion at a rate of 0.25 ml.min-1.kg-1 until the end of the experiment. Fifteen minutes after the start of the constant infusion the renal parameters were examined in 11 subsequent 15 min periods (the total time was 3 hours). Volume expansion produced no significant change in arterial blood pressure, glomerular filtration rate (GFR), plasma sodium and potassium concentration or, haematocrit, but did reduce the CPAH from 284 ml.min-1 to 218 ml.min-1 (the data were calculated for 100 gram wet kidney weight). There were constant significant increases in the urinary excretion rate from 0.84 ml.min-1 to 4.06 ml.min-1 and the 39% of the infused water was excreted during the experiment. Volume expansion also caused a significant increase in sodium excretion during the three first periods from 120 mumol.min-1 to 329 mumol.min-1 followed by a small but significant decrease. The sodium excretion at the end of the experiment was 221 mumol.min-1 and the 23% of the infused sodium was excreted in the course of the experiment. The increase of the water excretion during the volume expansion was associated with fall of the urine osmolality and the urine because hypoosmotic as compared to the plasma. We have provided evidence that vasopressin was not involved in the control of water excretion in our experiments. It is concluded that neither filtered sodium nor decreased aldosterone secretion can account for the increase in sodium excretion that occurs after Ringer solution loading in the dog. It has been proposed that a decrease in plasma protein concentration may decrease passive sodium reabsorption due to oncotic forces in the proximal tubule. The Ringer solution diuresis elicits a rise in medullary blood flow, thereby causing a washout of medullary sodium. This might dissipate the osmotic force for the back-diffusion of water from the collecting duct. Our studies indicate that the response of the diluting segments of the distal nephron to increased delivery of sodium depends upon the presence or absence of volume expansion. However the increase of the distal tubular loading activates the tubuloglomerular feedback which increases the proximal tubular reabsorption. Based on these assumptions our studies provide further evidence that the tubuloglomerular feedback regulates the blood pressure in the peritubular capillaries in the cortex around the proximal tubules.

Animals↗
PubMed1989

The effects of clonidine on the kidney function in the anesthetized dog.

Studies were performed to determine the mechanism by which the antihypertensive agent clonidine increased urine flow. The response of the kidney has been examined in four combinations. The parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution. In the control animals, volume expansion by 2% body weight, resulted in a slight increase in sodium excretion and urine flow. In 10 anesthetized dogs 1.0 microgram/kg/min of clonidine infused i.v. during 30 minutes (the total amount of clonidine infused was 30 micrograms/kg) decreased the arterial blood pressure from 136 +/- 13 mmHg to 127 +/- 12 mmHg and elevated urine flow from 2.95 +/- 1.65 ml/min to 4.34 +/- 1.77 ml/min while the urine osmolality diminished from 399 +/- 107 mosm/l to 265 +/- 90 mosm/l and the glomerular filtration remained constant. In 5 animals 0.1 microgram/kg/min of clonidine was infused into the left renal artery (this dose is corresponding to the renal fraction of the cardiac output) without any effects in the left kidney. 1.0 microgram/kg/min of clonidine infused directly into the left renal artery produced vasoconstriction in the ipsilateral kidney, decreased the glomerular filtration rate and the urine flow. By contrast in the right kidney the urine flow rose without hemodynamic changes, and the urine osmolality became hypoosmotic compared to the plasma. In ten dogs 1.0 microgram/kg/min of clonidine and 1 mU/kg/min of arginine-vasopressin were infused intravenously. The vasopressin infusion superimposed on the clonidine could not inhibit the increase of the urine excretion, and the fall of the urine osmolality. The results suggest that the clonidine increases the renal medullary blood flow possibly via a direct mechanism, decreases the sympathetic outflow to the kidney and via an indirect pathway, mediated by the renin-angiotensin system. The renal medullary flow increase produces a washout of the medullary osmotic gradient, and the water reabsorption diminishes.

Anesthesia↗
PubMed1988

The combined effects of dopamine (DA) and the DA antagonists EGYT-2509, chlorpromazine and haloperidol on the kidney function.

In anaesthetized dogs renal function was investigated in four successive 20-min periods in four experimental series. (1) In the first series following the first period (serving as control) 2.5 micrograms/kg/min of dopamine (DA) dissolved in 0.5 ml/min of Ringer's solution was infused into the left renal artery (period 2), than during periods 3 and 4. It was found that first (period 2) and second (period 3) doses of DA induced a significant decrease of about 20-30% in renal vascular resistance, and an increase of about 15-25% in renal blood flow. At the same time, systemic arterial blood pressure fell by 10%. The other investigated parameters of the left kidney (Cinulin, CPAH, sodium, potassium and water excretion) did not differ from the respective parameters of the intact right kidney. (2) In the second experimental series following the first period (prior to period 2) 1.0 mg/kg of the DA antagonist EGYT 2509 was administered intravenously. Prior to the period 3 again 1.0 mg/kg of EGYT 2509 and prior to period 4 2.0 mg/kg of EGYT 2509 was given intravenously. During periods 2 through 4 2.5 micrograms/kg/min of DA was infused into the left renal artery. It could be ascertained that EGYT 2509 abolished the renal effects of DA while not inducing any decrease in arterial blood pressure. (3) In the third experimental series, following the control period, prior to periods 2,3 and 4, 1.0 mg/kg, 1.0 mg/kg and 2.0 mg/kg chlorpromazine respectively, was administered i.v. followed by the infusion of DA into the left renal artery. After the administration of chlorpromazine arterial blood pressure and renal vascular resistance fell concomitantly and DA failed to induce any further changes in these parameters. According to our experiments chlorpromazine abolishes the effect of DA on kidney function. (4) In the fourth series, prior to DA infusion the dogs were given 0.5 mg/kg (period 2) then again 0.5 mg/kg and finally 1.0 mg/kg of haloperidol intravenously. Haloperidol decreased arterial blood pressure as well as renal vascular resistance, thus renal blood flow did not change. Renal blood flow could then be increased by DA infused into the left renal artery. It seems that haloperidol could not abolish the vascular effects of DA in the kidney. Our experiments indicate that substance EGYT 2509 possesses the most marked dopaminergic antagonistic effect, chlorpromazine had also been effective, while haloperidol had proved to be practically ineffective.

Animals↗
PubMed1984

A comparison of renal function following the infusion of Ringer solution into systemic and portal veins in the dog.

The increase of sodium and water excretion by the kidney following intravenous Ringer solution infused into a femoral vein (vena femoralis) or into an intestinal vein (vena portae ) has been studied in anaesthetized dogs. The functional parameters of renal function have been compared during volume expansion with 1.5-2.0% of body weight Ringer solution and "over-hydration" by 2.5% Ringer loading over 60 minutes. No significant difference in sodium excretion and urine output resulted from 0.25 ml/kg/min Ringer solution when infused by the two routes. When the animals were infused with 2.5% body weight Ringer solution (0.66 ml/kg/min i.v.), a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hyposmotic as compared with the plasma osmolarity. No difference has been found in the glomerular filtration rate and in the PAH clearance. Glomerular filtration rate, sodium excretion and urine flow rate were not significantly different for the two routes when the same Ringer solution load was infused. These experiments did not provide evidence for the participation of the liver in the control of sodium excretion during extracellular fluid volume expansion induced by Ringer solution infusion.

Animals↗
PubMed1983

Inhibition of prostaglandin synthesis and the action of vasopressin during extracellular volume expansion in the dog.

The increased renal sodium and water excretion after an intravenous infusion of Ringer solution has been investigated in anaesthetized dogs. The response of the kidneys has been examined in four combinations. The functional parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution and overhydration by 2.5% Ringer solution for 60 min. In the control animals, volume expansion by 2% body weight Ringer solution resulted in a significant increase in sodium excretion and urine flow. When these animals were infused with 2.5% body weight Ringer solution a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hypo-osmotic as compared to the plasma. No difference was found in glomerular filtration rate and PAH clearance. In the group No. 2, the effect of 4 mg/kg indomethacin infusion was studied. The inhibition of prostaglandin synthesis considerably reduced the diuretic effect of Ringer infusion and did not affect sodium excretion. In the group No. 3, the animals received lysine-8-vasopressin i.v. in a preliminary dose of 10 mU/kg during 10 min and then 50 mU/kg over 60 min in infusion. Volume expansion with 2.5% body weight of Ringer solution resulted in a marked increase in sodium and water excretion but no difference was found in glomerular filtration rate and PAH clearance. Dilution of the urine i.e. a decrease of urinary osmolarity, in spite of the vasopressin infusion, was significantly higher in this group than in the control animals (group No. 1). In the fourth series, after 4 mg/kg of indomethacin the same dose of vasopressin was administered as in group No. 3. Indomethacin was observed to inhibit the diuretic effect of vasopressin and did not affect the saluretic effect. From these data it was concluded that medullary tonicity affected renal water handling during extracellular isosmotic hypervolaemia induced by Ringer infusion. This mechanism depends on medullary prostaglandin synthesis and is independent from the plasma vasopressin concentration. Our findings clearly indicate that extracellular hypervolaemia increases renal sodium excretion and lysine-8-vasopressin was found to potentiate this effect. This sodium excretion increasing mechanism does not depend on renal prostaglandin secretion, nor were glomerular factors responsible for the increase of sodium and water excretion.

Animals↗
PubMed1982

Influence of augmentation of excretory renal mass on renal function after alpha-receptor blockade.

The effect of renal function of an augmentation of the excretory renal mass was investigated in 10 dogs without drug treatment and in 10 animals with alpha-receptor blockade. In the untreated group, augmentation of excretory renal mass by transplantation into the neck of one pair of kidneys isolated from another animal caused the following changes in the kidneys in situ: marked elevation in CPAH, slight decrease in Cinulin, slight diminution of urine excretion and a pronounced fall in sodium excretion. The amount of urine and sodium excreted by the four kidneys was identical with that previously excreted by the two kidneys in situ. In animals with alpha-receptor blockade, augmentation of the excretory renal mass had the following consequences in the in situ kidneys, CPAH, and Cinulin remained unchanged while urine and sodium excretion decreased to the same extent as in the untreated control group. The amount of urine and of sodium excreted by the four kidneys was the same as that excreted by the kidneys in situ, prior to transplantation of isolated kidneys, i.e. before the augmentation of excretory renal mass. It seems that the decrease in sodium excretion of the kidneys in situ was not due to the haemodynamic changes evoked by the load on the circulation; it was rather consequence of some quick, presumably humoral, regulation. The diminution of sodium excretion in the kidneys in situ after augmentation of the excretory renal mass has been ascribed to an increased utilization by the four kidneys of the natriuretic factor(s), i.e. to a diminution in the plasma level of the natriuretic hormone.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of indomethacin on renal function during different levels of surgical stress.

To determine whether renal prostaglandins participate in the regulation of renal blood flow, sodium and water excretion during "stress situation", renal function was investigated in two groups of anaesthetized dogs, subjected to minor and to more severe surgical stress under control conditions, and following the administration of 4 mg/kg indomethacin i.v. In the control studies, the renal haemodynamic parameters (CPAH, Cinulin), urine output and sodium excretion were not different in those animals in which the surgical traumatization was more severe from data obtained in similarly anaesthetized dogs. Extracellular volume expansion induced with i.v. infusion of Ringer solution enhanced sodium and water excretion in both groups, however, the increase of sodium excretion was less in the dogs subjected to more severe stress. During indomethacin infusion glomerular filtration did not change in either groups; CPAH decreased by 20-25% in the anaesthetized animals and 35-40% in dogs in which the surgical stress was more severe. In this group the total renal blood flow was reduced by 40% simultaneously with the haemodynamic changes; sodium and water excretion fell in both groups. After indomethacin infusion the diuretic response of the kidneys to extracellular volume expansion was markedly reduced in the anaesthetized dogs, the diuretic and natriuretic effects being almost completely inhibited in the animals subjected to more severe stress. These data suggest that in the anaesthetized dog endogenous prostaglandins may serve to maintain renal blood flow but not the glomerular filtration rate. Inhibition of prostaglandin synthesis during more severe stress results in increased renal vascular resistance and reduced renal blood flow. Accordingly, the data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during more severe surgical traumatization. The data do not support the direct physiological role of prostaglandins in regulating tubular function.

Animals↗
PubMed1982

Study of the indomethacin and bradykinin antagonism in anaesthetized dogs.

To determine the prostaglandin dependent and independent effects of bradykinin in the kidney, bradykinin (0.05 microgram/min/kg body weight) was infused into the left renal artery during inhibition of prostaglandin synthesis by indomethacin. Indomethacin, 0.1 mg/min/kg body weight i.v. produced a marked fall in urine output and sodium excretion in anaesthetized dogs. Renal vascular resistance increased and renal blood flow (RBFdir) decreased by 30%. When during the i.v. infusion of indomethacin bradykinin was infused into the left renal artery, RBFdir, urine flow and sodium excretion increased to the control values in the left kidney while remained lower in the right kidney. The results suggest that bradykinin increases renal blood flow by an action which does not require the mediation of prostaglandins. A decrease in renal blood flow, which was a constant feature during i.v. indomethacin infusion, is probably responsible for the decrease in urine flow and sodium excretion. The failure of indomethacin to inhibit the natriuretic and diuretic effects of bradykinin suggests that the prostaglandins are not important determinants of these responses.

Animals↗
PubMed1980

Effect on renal sodium and water excretion of the inhibition of prostaglandin synthesis in extracellular volume expansion.

In anaesthetized dogs the effect of the inhibition of prostaglandin synthesis on renal function was investigated in isosmotic extracellular volume (ECV) expansion of 1.5-2% of the body weight. The degree of ECV expansion was then elevated to about 5% of the body weight by infusing intravenously 25 ml/kg of Ringer solution within 60 minutes. Arterial blood pressure, glomerular filtration rate, CPAH, water and sodium excretion, urinary osmotic activity and Evans blue distribution space were determined in mild ECV expansion and during and after Ringer load. Prostaglandin synthesis was inhibited by giving intravenously 4 mg/kg indomethacin in ten minutes. A group of animals, receiving no indomethacin only the solvent, served as control. Indomethacin induced first a fast and afterwards a slow continuous increase in arterial blood pressure. In the control group, arterial blood pressure did not change. Glomerular filtration rate was similar in both groups throughout the whole experiment. In mild ECV expansion indomethacin decreased the PAH clearance, and renal sodium and water excretion, and elevated urinary osmotic activity as compared to the control group. During an ECV expansion of about 5% of body weight, in the control group water excretion exceeded three-fold the initial value, while sodium excretion increased only by 50% and urinary osmotic activity decreased below that of the plasma. The Evans blue distribution space increased significantly. In the indomethacin-treated animals, urine excretion increased to double the initial value, sodium excretion was similar as in the control group, and urinary osmotic activity much higher than in the control group. The Evans blue distribution space was practically unaffected by the Ringer load. In the after-load periods, the parameters investigated came nearer to each other but there was still a marked difference between the control and the indomethacin treated group at the end of the experiment. Indomethacin reduced the increase of urinary excretion under the effect of ECV expansion; control animals excreted 42.8 +/- 11.6%, while the indomethacin-treated dogs excreted only 30.2 +/- 17.6% of the water load. The alteration in renal function observed under the effect of indomethacin is attributed to functional changes in different parts of the nephron, arising probably in consequence of changes in cortical and medullary blood flow.

Animals↗
PubMed1978

Effect of increased excretory renal mass on kidney function.

Renal function was investigated in non-hydrated normal dogs and in dogs with slight isotonic hypervolaemia before and after increasing the excreting renal mass by connecting a pair of isolated kidneys into their circulation. After connecting the isolated kidneys to the perfusor's circulation, the excreting capacity of the in situ kidneys decreased markedly in both groups, without any change in the arterial blood pressure. Their urine output calculated for 100g kidney weight dropped from 0.52 +/- 0.43 to 0.30 +/- 0.18 ml/min in the non-hydrated group, and from 2.3 +/- 1.17 to 1.33 +/- 0.96 ml/min in the hydrated one. The urine flow of the isolated kidneys was 0.29 +/- 0.12 ml/min in the non-hydrated and 1.11 +/- 0.53 ml/min in the hydrated animals. Sodium excretion displayed similar changes. The findings suggest, that the excretory capacity of the kidneys and its distribution between the two kidneys is regulated very precisely. In our opinion, one or more "natriuretic factor" may be responsible for this precise regulation. The supposed factor seems to be produced extrarenally, and is only "used up" by the kidneys. It appears to exert its effect on the tubular part of the nephron, regulating the permeability of the tubular wall and controlling in this way the reflux of sodium and water from the capillary side to the tubular lumen. The decreased excreting capacity of the kidneys is attributed to an increased consumption of the natriuretic factor by four kidneys.

Animals↗
PubMed1977

The effect of indomethacin on kidney function: indomethacin and furosemide antagonism.

The effect of furosemide and indomethacin on renal function was investigated in anesthetized dogs. 1. On infusing 0.05 mg/kg/min furosemide directly into the left renal artery, about 18% of the filtered water and 19% of the filtered sodium was excreted in both non-hydrated and hydrated dogs. 2. Under the effect of 0.1 mg/kg/min indomethacin administered intravenously renal blood flow decreased markedly, glomerular filtration rate remained unchanged, the filtration fraction increased. 3. Indomethacin induced a decrease in water and sodium rejection and water and sodium excretion in both the hydrated and non-hydrated animals. 4. Indomethacin inhibited the diuretic effect of furosemide in the non-hydrated animals. This effect was much weaker in the hydrated group. These data suggest that in the anesthetized dog, endogenous prostaglandins may serve to maintain renal blood flow but not glomerular filtration rate. It is concluded that the indomethacin-induced inhibition of the furosemide effect is the consequence of hemodynamic changes occurring in the kidney. The data do not support the direct physiological role of prostaglandins in regulating tubular function.

Animals↗
PubMed1976

The effect of saline-induced extracellular volume expansion on the kidney function.

The functional parameters of renal function of non-hydrated and hydrated dogs (saline-infused to an extent of 1-2% of the body weight) have been compared. The directly measured renal blood flow and the total renal vascular resistance were the same in the two groups. No difference has been found in glomerular filtration rate, the Cinulin was the same in the two groups. There was no important difference in the PAH clearance and PAH extraction. In the hypervolaemic group, the sodium and water excretion was about threefold that of the non-hydrated animals. The plasma protein concentration was significantly lower in the hydrated group. In our experiments we did not find glomerular factors responsible for the increase of sodium and water excretion. The decrease of tubular reabsorption is attributed partly to the decreased plasma protein concentration, partly to unknown (perhaps natriuretic) humoral factors.

Animals↗
PubMed1976

Effect of sodium-ethylenediamine-tetraacetate on renal function.

Renal function was tested after decreasing the plasma ionized calcium level of renal artery. During EDTA infusion, renal blood flow (RBFdir) increased, while CPAH, Ccreat, EPAH and Ecreat decreased. In the left kidney, urinary and sodium excretion did not change significantly, while calcium excretion reached a fifteen-fold higher value than the control one. The unchanged urinary and sodium excretion in spite of the decreased glomerular filtration rate may have been due to the osmotic diuretic effect of the Ca-EDTA complex. The decrease of CPAH and EPAH was probably the consequence of a change in the secretory capacity in the absence of Ca++. the vasodilatation occurring in the efferent arterioles during EDTA infusion would serve to explain the decrease in the glomerular filtration rate. It is concluded that humoral vasoactive factors, mainly angiotensin, may have an important role in the regulation of the diameter of the efferent arterioles and in this way in the regulation of glomerular function.

Animals↗
PubMed1975

Changes in the water and sodium permeability of amphibian skin in the presence of the efferent plasma of "dehydrated dog kidney".

Two kidneys of the same dog were perfused separately with the same blood pool. After the control periods one of the kidneys was replaced by another one taken from a previously dehydrated dog. The presence of the "dehydrated kidney" resulted in a significant and almost immediate decrease in creatinin clearance of the contralateral perfused kidney. The Ccreat increased after the removal of the dehydrated kidney. Plasma samples were taken during the control, transplantation and recovery periods and their activity on the water permeability (osmotic water flow) and sodium transport was examined in amphibian skin. The presence of the plasma taken during the transplantation period resulted in a highly highly significant decrease in the osmotic water transport without any change in the sodium transport. This decrease was reversible, at least partly, after replacing the experimental plasma by a control one. These changes were not observed when a "desalted kidney" was used instead of the "dehydrated" one. These results suggest that in the status of dehydration the kidney releases some humoral factor or factors, which would induce a decrease in the measured GFR, possibly by a direct or indirect effect on membrane, probably glomerular membrane-permeability.

Animals↗