Intrauterine growth restriction reduces nephron number and renal excretory function in newborn piglets.

To examine the effects of intrauterine growth restriction on nephron number, renal circulation, and renal excretory functions in newborns, studies were conducted on 1-day-old anaesthetized piglets, divided into normal weight (n = 6) and intrauterine growth restricted (n = 6) piglets. Renal blood flow was measured by coloured microspheres, glomerular filtration rate was measured by inulin clearance, and osmotic clearance and fractional sodium excretion were calculated. In addition, an estimation of the nephron number was performed by counting representative glomerular numbers in microscopic sections. Newborn intrauterine growth restricted piglets exhibited a reduced glomerular filtration rate and osmotic clearance (P < 0.05), whereas renal blood flow and the filtration fraction as well as fractional sodium excretion were similar in normal weight and intrauterine growth restricted piglets. The nephron number was markedly reduced in intrauterine growth restricted piglets even if the nephron number was related to body weight (P < 0.01). There was a positive correlation between nephron number and glomerular filtration rate (r = 0.69, P < 0.05). Reduced glomerular filtration rate of newborn intrauterine growth restricted piglets is associated with a reduced nephron number. Thus, at birth, compensatory response of renal function due to nephron deficit does not exist in intrauterine growth restricted piglets.

The modification of rat liver regeneration by carcinogens and its reflection by extrahepatic tissues.

Liver regeneration is distinctly influenced by the treatment of male Sprague-Dawley rats with 2-acetylaminofluorene or N-methyl-N-nitrosourea on three successive days immediately prior to partial hepatectomy. The latter compound modulates the restorative liver growth, whereas it is strongly inhibited by the hepato-carcinogen 2-acetylaminofluorene. According to their influence on the regenerating liver, both carcinogens delay the post-operative decrease as well as the recovery of the physiological cell renewal in the jejunal and esophageal epithelium. Beside this, the circadian mitotic fluctuation of the esophagus is also altered by the carcinogens after partial hepatectomy like that of the regenerating liver. In contrast to the behaviour of the jejunum and the esophagus, the adrenocortical cell division is temporally elevated by the growth stimulus after partial hepatectomy. This effect is also found after carcinogen pretreatment only. For that reason one can assume that carcinogens produce a growth stimulating response like partial hepatectomy, which is displayed by an increased cell replication in the adrenal cortex. Possibly this phenomenon reflects common systemic mechanisms which indicate the promotory action of partial hepatectomy and chemical promotors as well as that of carcinogens.