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J C Perazzo

Publications and source records attributed to J C Perazzo.

21 records · Page 2Linked to original sources

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).

Acute Kidney Injury↗

Tyrosine hydroxilase activity in discrete brain regions from prehepatic portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertension in patients and rat models are characterized by splanchnic and systemic hemodynamic alterations. Both the central and autonomic nervous systems are implicated in its pathophysiology. The aim of our research was to study the tyrosine hydroxylase activity and the rate limiting step in the biosynthesis of catecholamines in partial ligated portal hypertensive and in control rat brains. METHODOLOGY: The following seven discrete brain regions were investigated: Subfornical Organ, Organum Vasculosum Lamina Terminalis, Median Eminence, Periventricular Nucleus, Area Postrema, Locus Coeruleus and Nucleus Tractus Solitarius. RESULTS: The enzyme activity showed a significant increment in six nuclei and a decrease in Area Postrema Nucleus when portal hypertensive rats were compared to controls. CONCLUSIONS: These results suggest the participation of some discrete brain regions in the mechanism of hepatic portal hypertension under the present rat model.

Animals↗