Kliegman R M
Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Childrens Hospital, Cleveland, Ohio 44106.
Pediatr Res. 1988 Nov;24(5):649-52. doi: 10.1203/00006450-198811000-00022.
The cerebral metabolic effects of hypoglycemia due to intrauterine growth retardation were studied in newborn dogs. Intrauterine growth retardation was induced in newborn dogs after 3 days of maternal nutritional deprivation (birth weight 251 +/- 7 versus 227 +/- 7 g, p less than 0.01). After birth, growth retarded pups developed fasting neonatal hypoglycemia which lasted from 3 to 9 h of life. The cerebral arteriovenous differences for glucose, oxygen, and ketone bodies were not different between growth-retarded pups or those from age-matched controls. The cerebral venous efflux of lactate was reduced, whereas the extraction of glucose (relative to blood glucose) was enhanced among growth-retarded pups. Cerebral glycogen content was lower in pups with growth retardation whereas phosphoenolpyruvate and pyruvate concentrations were augmented among growth-retarded pups. The latter may reflect a more oxidized cytoplasmic redox state but may also be due to diminished lactate efflux from the brain. Cerebral ATP content was not affected during periods of reduced blood glucose levels. These results suggest that in newborn dogs hypoglycemia associated with intrauterine growth retardation alters cerebral metabolism by increasing cerebral extraction of glucose and decreasing CNS efflux of lactate. We speculate that the net effect is increased lactate utilization within oxidative pathways and preservation of cerebral oxygen uptake. Cerebral glucose utilization is directed away from glycogen synthesis and toward glycolysis. Lactate oxidation rather than release to the systemic circulation may maintain cerebral ATP production in growth-retarded hypoglycemic newborn dogs.
对新生犬宫内生长迟缓所致低血糖的脑代谢效应进行了研究。在母体营养剥夺3天后诱导新生犬发生宫内生长迟缓（出生体重251±7克对227±7克，p<0.01）。出生后，生长迟缓的幼犬出现空腹新生儿低血糖，持续3至9小时。生长迟缓幼犬与年龄匹配对照组幼犬之间，葡萄糖、氧气和酮体的脑动静脉差异并无不同。生长迟缓幼犬的脑静脉乳酸流出量减少，而葡萄糖摄取（相对于血糖）增加。生长迟缓幼犬的脑糖原含量较低，而磷酸烯醇丙酮酸和丙酮酸浓度增加。后者可能反映了细胞质氧化还原状态的氧化程度更高，但也可能是由于脑乳酸流出减少所致。在血糖水平降低期间，脑ATP含量未受影响。这些结果表明，在新生犬中，与宫内生长迟缓相关的低血糖通过增加脑葡萄糖摄取和减少中枢神经系统乳酸流出而改变脑代谢。我们推测其净效应是增加氧化途径中乳酸的利用并维持脑氧摄取。脑葡萄糖利用从糖原合成转向糖酵解。乳酸氧化而非释放到体循环中可能维持生长迟缓低血糖新生犬的脑ATP生成。
