Acute renal failure induced by choline deficiency: structural-functional correlations.

The wide range of lesions obtained after feeding weanling rats with hypolipotropic diets underlies the interest of this model in the study of the pathophysiology of acute renal failure. Renal functional studies (experiment A) show that the more advanced grade of morphological alteration correlates well with a progressively more severe deterioration in renal function. In animals wtih morphological evidence of repair there was an evident rise in the urinary volume of a low osmolality and a reduction in blood urea. In experiment B, where the sequential changes in urine volume and composition were analyzed, the installation of the disease is marked by a decrease in body weight, food intake and water intake, a rise in urine Na concentration and by a fall in urine flow rate and renal capacity to excrete concentrated urine. The progressive decline in renal function observed in these animals would seem more linked to a primary tubular alteration which gradually becomes more extensive than with an initial ischemic alteration. The tubular necrosis can be interpreted as the initial lesion common to the wide morphological range observed in this model (tubular necrosis of various grades, cortical necrosis or evidence of repair).

In vivo and in vitro miniature end-plate potentials at various external K concentrations.

In order to obtain a nore reliable picture of transmitter release, spontaneous synaptic activity was studied in vivo in the rat soleus neuromuscular junction. The in vivo miniature end-plate potential (MEPP) recordings were compared with those obtained in vitro and, in both circumstances, MEPP frequency was measured at external potassiumconcentrations ranging from 5 to 15 mM. The influence of external potassium loading on intra- and extracellular potassium concentration also estimated by measuring the muscle ionic composition and water distribution at normal and high plasma potassium concentrations. The MEPP frequencies recorded in vivo were consistently lower than those observed in vitro for all external potassium concentrations studied (P less than0.01). These data suggest that better experimental conditions are maintained in thein vivo preparations, since the intracellular potassium increase that follows the external potassium loading can only partially justify the observed differnce and other factors, such as anesthetic effects, etc, may be ruled out.