EMBRYONIC RENAL INJURY: A POSSIBLE FACTOR IN FETAL MALNUTRITION

摘要: Chick embryo metabolism was monitored in a radlorespirometer where O2 consumption, CO2 production and 14CO2 from C-labeled proline, glutamate, aspartate arginine measured continuously during development. At nine days of development chemically dissimilar nephrotoxins (spermine, Na2 Cr2 O7, ethylene glycol monoethyl ether) were inoculated into the air sac which resulted temporary change respiratory quotient 0.71 to 0.85. 18 injured embryos consumed oxygen equal that 14 day 30-35% smaller weight. Embryos with renal injury but matched controls terms O2. utilization had profound decrease ability metabolize 14C-labeled substrates. Decreased proline associated decreased collagen formation. there pulmonary hypoplasia sparce mesenchyme maturation little residual evidence could be observed at ten days. It is suggested early fetal may alter gluconeogenesis addition interfering pathways essential for formation, thereby contributing malnutrition hypoplasia. Supported by N.I.H. Grant HD08864.