Experimental alteration of fetal growth in animals.
I have reviewed some of the experimental data related to nutritional and vascular experiments designed to produce intrauterine growth retardation in animals. While considerable effect of maternal nutritional deprivation can be seen in lower mammals, these effects tend to diminish or completely disappear in the nonhuman primate and possibly in the human. This does not mean that there are not nutritional influences that can be measured in the offspring, but that there appears to be a larger reserve in the higher order species. It is likely that the final common pathway for acquired intrauterine growth retardation is related to a compromise in the vascular supply at the uterine, placental, or umbilical levels resulting in a net decrease in the transport of oxygen as well as nutrients. Certain aspects of each of these experimental animal preparations such as the timing of the brain growth spurt in relation to the insult; the number of fetuses in the litter; the relative variability in growth parameters; the capacity for recovery and the specific end points examined, will influence the interpretation of results and allow for cautious extrapolation to the human problem of altered fetal growth. With the improvement in experimental techniques and equipment there should be more information forthcoming on blood flow studies and nutrient transport in a variety of chronic animal preparations.
D000818:Animals; D005314:Embryonic and Fetal Development; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology; D006168:Guinea Pigs / Q000378:metabolism; D000882:Haplorhini / Q000196:embryology; D007511:Ischemia; D008431:Maternal-Fetal Exchange; D009747:Nutritional Physiological Phenomena; D011247:Pregnancy; D011817:Rabbits / Q000196:embryology; D051381:Rats / Q000196:embryology; D012756:Sheep / Q000196:embryology; D013552:Swine / Q000196:embryology; D014599:Uterus / Q000098:blood supply