Gold A J, Costello L C
Am J Physiol. 1976 Jul;231(1):84-6. doi: 10.1152/ajplegacy.1976.231.1.84.
A model of steady-state hypocitricemia, characterized by hypocitraturia and reduced kidney cortex citrate, has been demonstrated in the rate chronically exposed to environmental heat. The renal citrate extraction ratio remains unchanged. The physiological mechanism that brings about the reduction in circulating citrate has not been determined. Hypocitraturia likely results from a decreased filtered citrate load. Although it is generally contended that filtered citrate load. Although it is generally contended that alkalosis increases and acidosis decreases renal excretion of citrate, observations of mild alkalosis and hypocitraturia during heat exposure suggest that factors other than pH can alter renal handling of citrate. Kidney mitochondrial function, as determined by in vitro measurements of citrate-stimulated respiratory rates and specific activities of isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and cytochrome c oxidase, appears to be unaffected by environmental heat.
在长期暴露于环境高温的大鼠中，已证实存在一种以低枸橼酸尿症和肾皮质枸橼酸盐减少为特征的稳态低枸橼酸血症模型。肾枸橼酸盐提取率保持不变。导致循环枸橼酸盐减少的生理机制尚未确定。低枸橼酸尿症可能是由于滤过的枸橼酸盐负荷减少所致。尽管一般认为碱中毒会增加而酸中毒会减少肾枸橼酸盐排泄，但热暴露期间轻度碱中毒和低枸橼酸尿症的观察结果表明，除pH值外的其他因素也可改变肾脏对枸橼酸盐的处理。通过体外测量枸橼酸盐刺激的呼吸速率以及异柠檬酸脱氢酶、琥珀酸脱氢酶、苹果酸脱氢酶和细胞色素c氧化酶的比活性来确定的肾线粒体功能，似乎不受环境高温的影响。
