Girard J R, Zeghal N
Biol Neonate. 1975;26(3-4):205-13. doi: 10.1159/000240731.
The adrenal epinephrine content of newborn rats delivered by caesarian section on day 21.5 of gestation and maintained at thermal neutrality (37 degrees C) did not decrease over the 6 h following birth in spite of a transient phase of hypoglycemia. Cold exposure (30 or 24 degrees C) of the newborn rats immediately after birth did not decrease their adrenal epinephrine content. A decrease in adrenal epinephrine content is observed in 21.5-day-old rat fetuses after insulin-induced hypoglycemia for 4 h, after 2-deoxy-D-glucose injection or after anoxia. In 20.5-day-old rat fetuses, insulin-induced hypoglycemia for 4 h or 2-deoxy-D-glucose did not decrease the adrenal epinephrine content of the fetus. No variation was observed in norepinephrine content of the adrenal gland in all these situations. It is concluded that spontaneously occurring hypoglycemia or cold exposure are not sufficient stimuli to induce adrenal epinephrine depletion. It is suggested that hypoxia is perhaps the physiological stimulus for epinephrine secretion in newborn rats.
在妊娠第21.5天通过剖腹产出生并维持在热中性（37摄氏度）的新生大鼠，尽管出生后有短暂的低血糖期，但在出生后的6小时内其肾上腺肾上腺素含量并未下降。新生大鼠出生后立即暴露于寒冷环境（30或24摄氏度）并不会降低其肾上腺肾上腺素含量。在胰岛素诱导低血糖4小时后、注射2-脱氧-D-葡萄糖后或缺氧后，观察到21.5日龄大鼠胎儿的肾上腺肾上腺素含量下降。在20.5日龄大鼠胎儿中，胰岛素诱导低血糖4小时或注射2-脱氧-D-葡萄糖并未降低胎儿的肾上腺肾上腺素含量。在所有这些情况下，肾上腺去甲肾上腺素含量均未观察到变化。结论是，自发发生的低血糖或寒冷暴露不足以刺激肾上腺肾上腺素耗竭。有人提出，缺氧可能是新生大鼠肾上腺素分泌的生理刺激因素。
