Abstract
The effects of experimental intrauterine growth retardation on subsequent fetal development, especially with respect to brain development, were studied in two groups of New Zealand white rabbits. The parameters investigated include wet weight, protein, DNA, protein/DNA, and the structure protein in myelin.
Experimental ischemia and subsequent fetal malnutriton were induced in the experimental group by litigation of spiral arterioles according to the method of Marthens and Harel. The results were that the brains in the malnurished fetuses revealed a significant decrease in weight, DNA, and protein content compared with those in the control group. However, there was no significant difference in the mean cell size index (protein/DNA) between the experimental group and the control group. DM-20 protein, proteolipid protein (PLP), and basic protein (BP) were present in all stages of development in both groups, although, unlike the experimental group, there was a gradual increase in the amount of these proteins in myelin from the 26 th to the 30 th day of gestation in the control group. On the other hand, high molecular weight proteins in myelin decreased more rapidly in the control group than in the experimental group during this same period of gestation. Experimental ischemia also caused a significant decrease in liver glycogen in the experimental group but not in the control group.
It was concluded that an inhibition of protein synthesis in the vulnerable period of brain development could lead to changes in brain structure, defects in cell growth, and failure in myelination.
