Experimental Growth Retardation in Rhesus Monkeys
1974; Wiley; Linguagem: Inglês
10.1002/9780470720097.ch7
ISSN1935-4657
Autores Tópico(s)Primate Behavior and Ecology
ResumoChapter 7 Experimental Growth Retardation in Rhesus Monkeys Donald E. Hill, Donald E. Hill Research institute and the Department of Pediatrics, Hospital for Sick Children, TorontoSearch for more papers by this author Donald E. Hill, Donald E. Hill Research institute and the Department of Pediatrics, Hospital for Sick Children, TorontoSearch for more papers by this author Book Editor(s):Katherine Elliott, Katherine ElliottSearch for more papers by this authorJulie Knight, Julie KnightSearch for more papers by this author First published: 01 January 1974 https://doi.org/10.1002/9780470720097.ch7Citations: 9Book Series:Novartis Foundation Symposia AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onEmailFacebookTwitterLinkedInRedditWechat Summary Intrauterine growth retardation has been produced in rhesus monkeys by experimental placental insufficiency. The growth-retarded newborns at term show morphological and biochemical alterations similar to those of growth-retarded human newborns. Organ weights followed the pattern seen in experiments on smaller mammals and in humans, with relative sparing of the brain and severe involvement of the liver and spleen. The newborn monkeys had reduced muscle mass and less fat in the carcass. In the brain, the changes in the cerebrum were minimal with a significant reduction in wet weight but no significant change in DNA, RNA and protein content. The changes in the cerebellum were greater than in the cerebrum and there were significantly low values for wet weight, total DNA, total RNA and total protein. In the liver, the concentration of DNA was unchanged but the total amount of DNA, RNA and protein was significantly low. The protein: DNA ratio was unchanged. The percentages of water, fat, and glycogen were similar to control values, but total amounts were significantly low. In muscle, the total DNA and the protein: DNA ratio were both extremely low, indicating a reduction in both cell size and cell number. The placenta in the growth-retarded monkeys weighed less than 110 g and this correlated well with the low birth weight. These findings indicate that a useful experimental model for studying various aspects of fetal growth retardation can be produced by vascular insufficiency. Although the mechanism of production is not comparable with that in the human disorder, many of the morphological and biochemical changes are similar to those occurring in growth-retarded human newborns. Further studies are in progress using this model for the determination of glucose homeostasis and postnatal catch-up growth. References Alexander, G. (1964). Studies on the placenta of the sheep (Ovis aries L.). Effect of surgical reduction in the number of caruncles. J. Reprod. 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