Mortola J P, Naso L
Department of Physiology, McGill University, Montreal, Quebec, Canada H3G 1Y6.
J Appl Physiol (1985). 1998 Jul;85(1):84-90. doi: 10.1152/jappl.1998.85.1.84.
Oxygen consumption (VO2) was measured in normoxia as ambient temperature (Ta) was lowered from 40 to 15 degrees C, at the rate of 0.5 degrees C/min (thermoneutrality approximately 33 degrees C). In 2-day-old rats born in hypoxia after hypoxic gestation, the Ta-VO2 relationship was as in controls; their interscapular brown adipose tissue (IBAT) was hypoplastic (less proteins and DNA), with lower concentration of the mitochondrial uncoupling protein thermogenin. In 8-day-old rats exposed to hypoxia postnatally (day 2 to day 8), at any Ta below thermoneutrality VO2 was higher than in controls; also, in this group IBAT was hypoplastic with decreased thermogenin. Additional measurements under various experimental conditions indicated that the increased thermogenic capacity was not explained by the smaller body mass and increased blood oxygen content or by the eventuality of intermittent cold stimuli during the chronic hypoxia. On the other hand, chronic hypercapnia (3% CO2 in normoxia, from day 2 to day 8) also resulted in increased normoxic thermogenesis. We conclude that chronic hypoxia in the perinatal period 1) reduces IBAT mass and thermogenin concentration and 2) can increase the newborn's thermogenic capacity because of stress-related mechanisms not specific to hypoxia.
在常氧条件下，将环境温度（Ta）以0.5℃/分钟的速率从40℃降至15℃（热中性温度约为33℃），并测量氧耗量（VO2）。对于孕期缺氧后出生的2日龄大鼠，其Ta-VO2关系与对照组相同；它们的肩胛间棕色脂肪组织（IBAT）发育不全（蛋白质和DNA含量较少），线粒体解偶联蛋白产热素的浓度较低。对于出生后（第2天至第8天）暴露于缺氧环境的8日龄大鼠，在任何低于热中性温度的Ta下，其VO2均高于对照组；此外，该组大鼠的IBAT也发育不全，产热素减少。在各种实验条件下的额外测量表明，产热能力的增加不能用体重较小、血氧含量增加或慢性缺氧期间间歇性冷刺激的可能性来解释。另一方面，慢性高碳酸血症（常氧条件下3%的二氧化碳，从第2天至第8天）也导致常氧条件下的产热增加。我们得出结论，围产期的慢性缺氧1）会减少IBAT的质量和产热素浓度，2）并且由于与应激相关而非特定于缺氧的机制，会增加新生儿的产热能力。
