Perinatal changes in glycolytic function in response to hypoxia in the incubated or perfused rat heart.
Perinatal changes in glycolytic function in response to hypoxia in the incubated or perfused rat heart.
复制标题
围产期糖酵解功能因孵化或灌注大鼠心脏缺氧而发生变化。
DOI：
10.1159/000241064
复制
发表时间：
1978
期刊：
影响因子：
--
通讯作者：
L. Opie
中科院分区：
文献类型：
--
作者：
J. Hoerter;L. Opie
在围产期大鼠心脏中评估糖酵解：在产后16.5天（dpc）和21.5 dpc（term = 22 dpc）的胎儿中，以及在产后1天（dpp）和7 dpp的新生儿中。葡萄糖的摄取，乳酸的产生和葡萄糖纳入糖原在胎儿比在新生儿的心脏要高得多。测量了高能磷酸化合物、乳酸盐和己糖磷酸盐的组织含量。在缺氧过程中，尽管通过磷酸果糖激酶（PFK）的流量增加，但葡萄糖-6-磷酸和果糖-6-磷酸的含量不变，表明PFK早在16.5 dpc就在糖酵解中起调节作用。离体胎心比新生儿心脏更耐缺氧：葡萄糖摄取和乳酸产生更高，高能磷酸化合物和糖原在胎心中得到更好的维持。
Glycolysis was assessed in the rat heart during the perinatal period: in the fetus of 16.5 days postcoitum (dpc) and 21.5 dpc (term = 22 dpc) and in the newborn of 1 day postpartum (dpp) and 7 dpp. Glucose uptake, lactate production and glucose incorporation into glycogen were much higher in the fetal than in the newborn heart. Measurements were made of tissue contents of high energy phosphate compounds, lactate and hexose phosphates. Unchanged contents of glucose-6-phosphate and fructose-6-phosphate during hypoxia in spite of an increased flux through the enzyme phosphofructokinase (PFK) suggest that PFK has a regulatory role in the glycolysis as early as 16.5 dpc. The isolated fetal heart was more resistant to hypoxia than the newborn heart: glucose uptake and lactate production were much higher and high energy phosphate compounds and glycogen were better maintained in the fetal heart.