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F Stephan

Publications and source records attributed to F Stephan.

At least 55 records · Page 3Linked to original sources

[Effects of fasting and of ACTH on renal compensatory hypertrophy in the 48 hour uninephrectomized rat].

Renal compensatory hypertrophy (R.C.H.) is determined 48 h. after uninephrectomy in fed and fasting rats having free access to a NaCl solution. ACTH (18 gamma/100 g BW/d/2d) enhances R.C.H. in the fed animals. R.C.H. is severely impaired by food deprivation and the remaining kidney looses weight; a normal kidney weight can be maintained if the fasted, uninephrectomized rat is treated with ACTH. These experiments suggest that the stimulation of the adrenal cortex by ACTH has a renotrophic effect. This action may be related to the elevation of blood glucose or/and to the fall of the concentration of plasma K+.

Adrenal Cortex↗

[Inhibition of compensatory kidney hypertrophy by hypothyroidism in the rat. Measurement of the mean diameter of glomeruli and proximal tubules].

The body, heart and kidney weights are reduced in the hypothyroid rat. In this animal, the diameter of the proximal tubule is significantly smaller than in euthyroid controls. The glomerular diameter is not affected by hypothyroidism. 21 days after uninephrectomy, the weight of the remaining kidney and the diameter of the proximal tubule increase significantly both in the hypothyroid and the euthyroid rats. But this compensatory renal hyperthrophy is definitely impaired in the hypothyroid animals.

Animals↗

[Tooth regeneration in the guinea pig (Cavia porcellus)].

The first inferior molar has been extracted, a part of its being reimplanted or not. A new molar of normal form regenerated, apparently from the apex of the tooth germ, in all cases in which the alveolus was left free or implanted with a tooth freagment deprived of pulpa.

Animals↗

[Enhancement of compensatory renal hypertrophy by beta-1-24 corticotropin in the rat].

In the rat, the administration of beta1-24-corticotrophin during 7 days following an uninephrectomy enhances significantly the compensatory hypertrophy of the remaining kidney. There is no increase in renal compensatory hypertrophy when ACTH is injected to previously adrenalectomized rats. This action of ACTH could be related to the diabetes mellitus induced by this hormone or to an increase in sodium reabsorption by the tubular epithelial cells.

Adrenal Glands↗

[Excretion of water, sodium, and potassium during the compensatory renal hypertrophy in hypothyroid rats].

Renal compensatory hypertrophy is studied in age matched euthyroid and radiothyroidectomized female rats. 7 days after uninephrectomy, the hypertrophy of the remaining kidney is equally small in both groups. But 60 days after this operation, the hypothyroid animals show only a 12% increase in the wet weight of the remaining kidney whereas the euthyroid controls increase this weight by 21%. The excretion of water, Na and K are determined in the urine excreted in 5 h after a small water load. The results are related to 1 gram of kidney wet weight. These outputs increase in all animals after uninephrectomy. They are significantly higher in the hypothyroid rats than in the euthyroid controls as well before than 60 days after uninephrectomy. The reduction in tubular Na reabsorption found in the hypothyroid rat may account for the impairment of compensatory renal hypertrophy in hypothyroidism.

Animals↗