摘要:

The effect of prolonged hypoxia, transient and prolonged hypotension, and of acidosis on rat kidney and muscle water, sodium, potassium, magnesium, and phosphate composition was investigated. A significant increase in kidney tissue water was found in all experimental groups. Prolonged hypotension produced a decrease in kidney potassium and magnesium content and an increase in sodium content. Hypoxia produced an increase in magnesium content. No significant changes in the kidney solutes measured resulted from transient hypotension or respiratory acidosis. Skeletal muscle water was increased in all but the hypoxic group and potassium content in all but the prolonged hypotension group. It is suggested that prolonged hypotension results in renal depletion of normal intra-cellular cations and replacement by sodium. These changes probably indicate loss of functional integrity of renal cells and may relate to the clinical syndrome of acute tubular necrosis and to delayed function of homografted cadaver kidneys.

ISSN:1660-8151    

DOI:10.1159/000179804

出版商:S. Karger AG    

年代:1970

数据来源: Karger

摘要:

L’infusion intraveineuse massive de solution saline isotonique chez le chien entraîne une réduction de la réabsorption tubulaire de sodium, observée indépendamment de toute variation de la quantité de sodium filtrée. Une relation linéaire inverse est décrite entre la natriurie et la pression oncotique péritubulaire. Cette relation n’est pas influencée dans sa structure (coefficient angulaire) par l’administration préalable de substances susceptibles de déprimer le transport actif du sodium par la cellule tubulaire (organomercuriel et spironolactone) administrées seules ou en association. Cette constatation est interprétée comme un argument en faveur de l’existence de la réabsorption d’une faible fraction du sodium filtré par un processus dependant du gradient de pression oncotique transtubulaire. Cette hypothèse est confrontée avec les diverses théories actuellement proposées pou

ISSN:1660-8151    

DOI:10.1159/000179805

出版商:S. Karger AG    

年代:1970

数据来源: Karger

摘要:

The pattern of respiratory compensation in chronic uremic acidosis has been delineated on the basis of an analysis of 145 determinations of the arterial acid base status of 19 patients suffering from terminal renal failure and treated by chronic hemodialysis. In the bicarbonate range studied (11–21 mEq/l) it was shown that pCO2 was linearly related to plasma bicarbonate concentration (pCO2 = 1.214 HCO-3 + 10.87), whereas blood hydrogen ion concentration rises in a curvilinear fashion with decreasing plasma bicarbonate concentration. Significance bands enabling the prediction of the physiological ventilatory response to chronic metabolic acidosis were calculated from these data. An analysis of the individual ventilatory response to metabolic acidosis was made in 10 patients. No difference was found between the slopes of the pCO2 response lines whereas the elevations of the lines were shown to vary from individual to individual. This suggests that every subject has his own threshold of sensitivity to metabolic acidosis. Between two dialyses, plasma bicarbonate concentration fell linearly as a function of time, at a rate of 1.9 mEq/l per day. The effect of dialysis on the ventilatory response to acidosis was evaluated on the basis of an analysis of 96 determinations of the arterial acid base status performed immediately after dialysis. It was shown that a 12 h dialysis did not modify the linearity nor the slope of the pCO2 bicarbonate relationship but decreased its elevation (pC02= 1.203 HCO-3+ 7.67 ± 2.4

ISSN:1660-8151    

DOI:10.1159/000179806

出版商:S. Karger AG    

年代:1970

数据来源: Karger

摘要:

Experiments in the acidotic and alkalotic dog were performed to provide information on the properties of luminal and antiluminal transport for plasma glutamine and the relationship of renal hemodynamics to production of ammonia. In titration experiments, luminal transport, i.e. reabsorption of glutamine, was essentially complete in both acidosis and alkalosis over a tenfold range of plasma concentration. As higher plasma concentrations resulted in renal vascular collapse no direct evidence for a Tm limitation of transport capacity could be obtained. Antiluminal transport of glutamine from peritubular blood was observed in 5 out of 6 experiments in chronic metabolic acidosis. Renal production of ammonia was essentially equal to that derived from reabsorbed glutamine plus that transported across antiluminal membranes and equally well correlated with renal blood flow and filtration rate. We conclude that in chronic metabolic acidosis glutamine which enters tubular cells across antiluminal membranes as well as that which enters across luminal membranes is utilized for the production of ammonia.

ISSN:1660-8151    

DOI:10.1159/000179807

出版商:S. Karger AG    

年代:1970

数据来源: Karger

摘要:

The higher J GI in the outer renal cortex of dog and beaver as compared to the juxtamedullary cortex indicates that the distribution of the JG cell granularity does not depend entirely on the length of the Henle loops, but could be, in part, related to the size of the glomeruli in relation to the deepness of the renal cortex.

ISSN:1660-8151    

DOI:10.1159/000179808

出版商:S. Karger AG    

年代:1970

数据来源: Karger

摘要:

Rats depleted of renin by chronic saline loading are largely protected from glycerol induced acute renal failure. For some 4 h after glycerol injection, these animals showed the same apparent renal ischemia, cessation of filtration and tubule collapse seen in rats that are not renin depleted. Despite this ischemia, renal function returned rapidly, individual nephron GFR reaching 75 % of normal within the succeeding 12 h. Significant outflow obstruction was evident transiently early in recovery, but was found not to be the prime cause of the low GFR. Recovery of glomerular filtration occurred quickly despite the presence of grossly elevated hydrostatic pressure in some nephrons. It is suggested that renin depletion produced by long term saline ingestion may prevent the protracted afferent arteriolar constriction which is chiefly responsible for the pathophysiologic events in this model of acute renal failure in the rat.

ISSN:1660-8151    

DOI:10.1159/000179809

出版商:S. Karger AG    

年代:1970

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000179810

出版商:S. Karger AG    

年代:1970

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000179811

出版商:S. Karger AG    

年代:1970

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000179812

出版商:S. Karger AG    

年代:1970

数据来源: Karger