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Biomedical subjects

E Szöcs

Publications and source records attributed to E Szöcs.

At least 19 recordsLinked to original sources

Intrarenal haemodynamics in uranyl nitrate-induced acute renal failure.

Intrarenal haemodynamics were investigated in the dog at various intervals after the iv. injection of 10 mg/kg uranyl nitrate (UN). Renal blood flow (RBF), as determined by measuring the renal venous effluent and by radioactive microspheres, decreased by about 23% at 6 hr after UN administration, as compared to normal controls, then rose and reached controls at 24 to 48 hr; subsequently, RBF increased and surpassed controls by about 36% at 96 hr. Thus, the early phase (6 hr) and the late phase (96 hr) of uranyl nitrate-induced acute renal failure (UNARF) were characterized by an increase and by a decrease, respectively, in overall renal vascular resistance. Glomerular filtration rate (GFR) diminished to about 37% of controls at 6 hr, with no change in urinary output (V). In the following hours, however, GFR and V fell quickly and reached practically zero at 12 to 24 hr. Approximate calculations revealed a predominantly preglomerular vasoconstriction in the early phase and post-glomerular vasodilatation in the late phase. Radioactive microspheres showed a nearly proportionate decrease in perfusion of all cortical layers in the early phase (6 hr); in the late phase (96 hr), however, blood flow to the outermost layer remained unaltered, while perfusion of the inner cortical and juxtamedullary layers increased significantly.

Acute Kidney Injury↗

Functional changes in compensatory hypertrophy of the canine kidney after uninephrectomy.

Kidney weight and renal functional parameters were investigated in dogs 7 to 68 days after uninephrectomy. Average enlargement of the remaining kidney amounted to 35.1%. Renal blood flow (RBF) and glomerular filtration rate (GFR) calculated per 100 g actual kidney weight were identical in the non-hypertrophied controls and in the hypertrophied kidneys, i.e. structural and functional changes were strictly proportional. Calculation of mean nephron parameters (MNRBF and MNGFR) revealed an increase of about 43% in the hypertrophied kidneys, with an appropriate decrease in nephronal vascular resistance. The hypertrophied kidney showed an enhanced responsiveness to mannitol; increased MNRBF under stop flow conditions was due to a pronounced dilatation of the postglomerular vessels. There was no difference between control and hypertrophied kidneys in cortical zonal blood flow, as investigated by the labelled microsphere technique. Increase in parallel-connected cortical resistances towards the inner (juxtamedullary) zones was pronounced.

Adaptation, Physiological↗

Pathomechanism of postischaemic renal failure in the dog induced by temporary occlusion of the renal artery.

Intrarenal haemodynamics were investigated in previously uninephrectomized dogs, immediately after release and on the third day following two hours clamping of the renal artery. Postischaemic renal failure (PIRF) was considered moderate or severe, if three days after clamping plasma NPN values were under or over 150 mg/dl, respectively. Renal blood flow (RBF) as determined by measuring the renal venous effluent and by radioactive microspheres did not differ significantly from controls either immediately after release, or three days following arterial occlusion. Glomerular filtration rate (GFR) was, however, severely depressed in all postischaemic kidneys. An increase in preglomerular and a decrease in postglomerular resistance was assumed, resulting in unaltered total vascular resistance and a sharp drop in glomerular capillary pressure. Radioactive microspheres revealed a shifting of intrarenal blood flow from the superficial cortex towards the deeper (juxtamedullary) cortical layers. Fractional flow to the outer cortex was decreased, that to the inner cortex increased, as compared with uninephrectomized controls.

Acute Kidney Injury↗

Renal haemodynamics in mercuric chloride-poisoned dogs.

Intrarenal haemodynamics and glomerular dynamics have been investigated in dogs with mercuric chloride-induced acute renal failure. The early phase (12 and 24 hr after the intravenous injection of 2 mg/kg HgCl2) is characterized by some decrease in renal bloodflow, due to afferent (preglomerular) vasoconstriction, while in the later phase (48 and 72 hr after poisoning a pronounced increase in RBF due to efferent (postglomerular) vasodilatation supervenes. Urinary volumes amounts to normal in the early phase, followed by oligo-anuria in the 48 and 72 hr groups. Extraction ratio of inulin, i.e. the filtration fraction and, consequently, glomerular filtration rate show a progessive decline and trend towards zero in the 72 hr group. The pronounced decrease in glomerular capillary pressure is due to both absolute and relative increase and decrease in afferent and efferent resistances, repectively. The progressive fall in effective filtration pressure is brought about by the decrease of glomerular capillary pressure, combined with increased colloid osmotic pressure due to haemoconcentration. Total and segmental intrarenal vascular resistances are reduced by hyperosmotic mannitol infusions resulting in renal hyperaemia. Glomerular filtration rate is, however, not influenced by mannitol and effective filtration pressure remains unaltered. Osmotic diuresis ensues in the early phase but urinary output is not restored in the late, i.e. oligo-anuric, phase.

Acute Kidney Injury↗

Renal haemodynamics in dogs with dehydration azotaemia.

Intrarenal pressure gradients and glomerular dynamics have been investigated in dogs with severe dehydration elicited by pyloric ligation. 1. Because of the proportionate decrease in arterial pressure and renal blood flow, calculated total renal vascular resistance was found unaltered as compared with normohydrated controls. The slight changes in series connected intrarenal resistances were not significant. 2. Net hydrostatic pressure across the glomerular membrane, i.e. glomerular capillary minus proximal tubular pressure was slightly diminished. The pronounced fall in effective filtration pressure was due to the considerable increase in colloid osmotic pressure of the plasma proteins. 3. Reduced arterial pressure due to clamping of the aorta did not diminish vascular resistance. Thus, the autoregulatory capacity of renal circulation seems to be lost in dehydrated animals. 4. No correlation was found between plasma NPN values on the one hand and RBF and GFR on the other. Azotaemia seemed to be due to retention and enhanced rediffusion of urea and increased katabolism of tissue proteins. 5. Reduced urine flow caused by dehydration was restored by isosmotic saline or hyperosmotic mannitol infusions. Both agents act by decreasing intrarenal vascular resistance and by diminishing the increased colloid osmotic pressure.

Animals↗