Search PubMed⌕ Search

Biomedical subjects

N G Levinsky

Publications and source records attributed to N G Levinsky.

At least 73 records · Page 4Linked to original sources
PubMed1974

Superficial and juxtamedullary nephron function during saline loading in the dog.

A modification of the microdissection technique of Hanssen was utilized in dogs to measure superficial (SNGFR) and juxtamedullary nephron filtration rate (JMGFR) in control and saline-expanded dogs. During control studies SNGFR was 60+/-4 and JMGFR was 72+/-5 nl/min. During saline loading SNGFR was 74+/-8 and JMGFR was 65+/-6 nl/min. The ratio SNGFR: JMGFR significantly increased from 0.84+/-0.03 to 1.15+/-0.08. Glomerular perfusion rate (GPR) was measured with the microsphere method during control and saline loading. Superficial GPR did not change significantly but juxtamedullary GPR increased from 225+/-42 to 323+/-39 nl/min. Calculated superficial nephron filtration fraction was unchanged after saline expansion but juxtamedullary filtration fraction decreased from 0.34+/-0.07 to 0.24+/-0.07. The data demonstrate a tendency for filtration to shift toward the superficial part and plasma flow toward the deep part of the kidney cortex. GFR in juxtamedullary nephrons appears to be less plasma flow-dependent than in superficial nephrons. The fall in filtration fraction in the deep cortex may affect sodium excretion by juxtamedullary nephrons.

Animals↗
PubMed1972

Restoration and maintenance of glomerular filtration by mannitol during hypoperfusion of the kidney.

Glomerular filtration (GF) during progressive reduction of renal perfusion pressure by aortic clamping was studied in hydropenic rats and in rats infused with isotonic saline, hypertonic saline, or mannitol. As judged by visual observation of Lissamine green movements in superficial nephrons. GF was absent in hydropenic or saline-loaded rats at 40 mm Hg aortic pressure, but continued in some nephrons of all rats infused with mannitol and of some rats infused with hypertonic saline. Urine flow persisted only in rats infused with mannitol. By use of the qualitative Hanssen technique, it was found that all glomeruli in superficial and deep portions of the cortex were perfused at 40 mm Hg in all groups of rats. By the same method. GF continued in 1% of nephrons in hydropenic rats, 12% of nephrons in isotonic saline-loaded rats, and 78% of nephrons in rats infused with mannitol. By means of a quantitative Hanssen technique, GF was 5.8 nl/min per nephron in mannitol-infused rats and not measurable (< 0.5 nl) in hydropenic rats. Superficial and deep nephrons were similar in both qualitative and quantitative studies. Although urine flow did not persist in rats infused with hypertonic saline, GF was detected in four of seven studies by the Hanssen method (mean, 9.1 nl/min per nephron). In additional experiments, mannitol infused after perfusion pressure had already been lowered to 40 mm Hg in hydropenic rats reestablished urine flow and GF (mean, 9.8 nl/min). Furosemide, isotonic and hypertonic saline did not restart urine flow; however, GF (Lissamine green) was restarted by hypertonic saline. We conclude that mannitol can maintain or reestablish by an extratubular mechanism GF which otherwise would not occur during renal hypoperfusion. Hypertonic saline has a similar effect on GF in some cases, but urine flow is not maintained, implying complete reabsorption of filtrate.

Animals↗
PubMed1972

Tubular reabsorption of sodium during acute and chronic volume expansion in man.

Renal hemodynamics and tubular fractional sodium reabsorption (FSR) were evaluated by clearance techniques during acute and chronic extracellular volume expansion in man. (1 - V/GFR) x 100 was used as an index of proximal and (C(H2O)/V) x 100 as an estimate of distal fractional reabsorption. After acute loading with isotonic saline 37 ml/kg body wt, proximal FSR decreased by 4.8% and distal FSR decreased by 4.4%. After comparable chronic expansion by mineralocorticoids ("escape"), proximal FSR also decreased by 3.9%, but distal reabsorption was not altered.In separate studies, subjects were progressively infused with saline to 57 (E(1)) and to 80 (E(2)) ml/kg body wt, and appeared to divide into "excreters" (maximum U(Na)V > 1000 muEq/min) and "nonexcreters" (maximum U(Na)V < 550 muEq/min). In the excreters, GFR rose, proximal FSR decreased by 7.1% after E(1) and only 0.9% further after E(2). Distal FSR fell by 14.8% after E(1) and by an additional 4.9% after E(2). In the nonexcreters, GFR was stable and proximal FSR did not fall significantly after E(1) or E(2). Distal FSR decreased 4.5% after E(1) and 1.3% further after E(2). It is concluded that both acute and chronic extracellular expansion decrease proximal FSR in man, but only acute loading depresses distal FSR. Ability of some men to excrete sodium rapidly after acute infusion is related to larger increases in GFR and greater decreases in both proximal and distal FSR than occur in men in whom natriuresis is more limited.

Adult↗
PubMed1971

Proximal tubular function in dogs with thoracic caval constriction.

The effect of saline infusion on proximal sodium reabsorption was compared in normal dogs and in dogs with acute or chronic partial thoracic vena cava obstruction. After acute vena cava obstruction, proximal fractional sodium reabsorption rose by 74%. During continued caval obstruction, saline loading strikingly reduced proximal reabsorption but sodium excretion remained minimal. In chronic caval dogs, saline loading reduced proximal fractional sodium reabsorption by 31% but sodium excretion in the micropunctured kidney was only 41 muEq/min. After saline infusion in normal dogs, proximal fractional sodium reabsorption fell 39% while unilateral sodium excretion rose to 584 muEq/min. Nephron filtration rate was also measured before and after saline loading in normal and chronic caval dogs in both repunctured and fresh tubules. There was a marked increase in nephron filtration rate in repunctured tubules and no change in freshly punctured tubules in both groups. The effect of saline loading on nephron filtration rate in normal and chronic caval dogs was similar, therefore, whether repunctured or fresh nephrons were considered.We conclude that saline infusion depresses proximal sodium reabsorption in acute and chronic TVC dogs. Since saline loading markedly increases distal delivery without a concomitant natriuresis, enhanced distal reabsorption must play a major role in the sodium retention exhibited by chronic caval dogs. Redistribution of filtrate does not appear to be a factor in this sodium retention.

Aminohippuric Acids↗
PubMed1968

An extrarenal mechanism of potassium adaptation.

Rats fed a diet high in potassium for several days survive an acute load of potassium that is lethal to animals on a regular diet. Previous data suggested that this survival occurred because of enhanced kaluresis. Although increased urinary excretion may occur, the major mechanism of this potassium adaptation phenomenon has been found to be extrarenal. Despite nephrectomy just before study, rats previously fed a high potassium diet maintained lower plasma potassium concentrations for at least 2 hr after an acute potassium load than did rats fed a regular diet. Prior adrenalectomy abolished adaptation. Furthermore, rats fed a low sodium diet as an alternative stimulus to aldosterone secretion demonstrated adaptation to potassium loading, as did adrenalecomized rats given large doses of deoxycorticosterone for several days. Adrenalectomy just before the test load of potassium did not abolish adaptation nor did a large dose of aldosterone at that time reproduce it. These data indicate that adaptation is dependent on a chronic increase in aldosterone secretion. The extra potassium removed from the extracellular fluid by adapted rats was not lost into the gastrointestinal tract. It is concluded that more rapid lowering of plasma potassium after acute potassium loads by adapted rats is due to enhanced uptake of potassium by one or more tissues stimulated by chronic aldosteronism.

Adaptation, Physiological↗
PubMed1968

Renal excretion of urobilinogen in the dog.

The renal excretion of urobilinogen was studied in dogs by standard clearance techniques. The use of radiochemically pure tritiated mesobilirubinogen as a representative urobilinogen afforded much greater analytical precision than can be obtained with the usual colorimetric and fluorimetric techniques which are only semiquantitative. With constant plasma levels of urobilinogen, raising urinary pH from 5 to 8 increased urobilinogen excretion from about 30% to up to 200% of the filtered load. When urinary pH was kept constant, changes in blood pH had no effect on urobilinogen excretion. Increases in urinary flow had no effect on urobilinogen excretion when the urine was alkaline but increased excretion markedly during aciduria. Probenecid did not influence urobilinogen excretion by the kidney. It is concluded that urobilinogen is excreted by a three-component system of glomerular filtration, active secretion, and pH-dependent nonionic diffusion in the distal nephron. Urobilinogen is a weak acid, and this mode of excretion is similar to that of other weak, organic acids, such as salicylates. These results indicate that urinary pH and flow must be considered in the clinical interpretation of measurements of urinary urobilinogen.

Acidosis↗
PubMed1967

Evidence that an acute increase in glomerular filtration has little effect on sodium excretion in the dog unless extracellular volume is expanded.

The concept that acute increases in glomerular filtration rate (GFR) will cause large concomitant increases in sodium excretion has been re-examined. In previous work, GFR was elevated by volume expansion, usually with saline infusions. Recent evidence shows that tubular reabsorption is depressed during saline loading; hence, the independent effect of increased GFR on sodium excretion cannot be assessed.TO DETERMINE THE EFFECT OF ACUTE INCREASES IN GFR PER SE ON SODIUM EXCRETION, WE RAISED GFR BY FOUR TECHNIQUES NOT INVOLVING VOLUME EXPANSION: protein feeding, dopamine infusion, intravenous dexamethasone, and cross-circulation. GFR increased acutely by 5 to 85% in these experiments. In 12 of 24 experiments, GFR increased by more than 30%. In all but one experiment, sodium excretion increased by less than 75 muEq per minute. Data from experiments using each of the four techniques were comparable. The results were the same whether mineralocorticoid activity was high or low. In contrast, during saline loading, sodium excretion increased more than 800 muEq per minute with equal or lesser changes in GFR. These results demonstrate that acute increases in GFR per se have little effect on sodium excretion. We suggest that, due to constant fractional sodium reabsorption in the proximal tubule (glomerulotubular balance) and increased distal reabsorption, virtually all of the increase in filtered sodium is reabsorbed when GFR increases. Depression of tubular reabsorption is required for natriuresis.

Absorption↗