Stevenson D K, Ostrander C E, Johnson J D
J Lab Clin Med. 1979 Oct;94(4):649-54.
One of the major contributory factors to hyperbilirubinemia in the human infant is bilirubin production. Determination of the pulmonary excretion rate of carbon monoxide is used to measure indirectly the rate of bilirubin production by estimating the endogenous production of CO, which is formed in equimolar amounts with bilirubin in the catabolism of heme. There has been no study to confirm that complete recovery of CO produced in vivo from the catabolism of known amounts of heme occurs via pulmonary excretion. We report here quantitative determinations of the pulmonary excretion rate of CO in five adult male Wistar rats after injection of known amounts of heme in the form of red blood cells "damaged" by incubation in a solution containing a sulfhydryl inhibitor, NEM. The mean recovery of "extra" CO above baseline production represented as a molar ratio of extra CO to heme was 0.98 +/- 0.02 (S.E.). Control studies showed no extra CO production after starvation, injection of NEM in an amount comparable to that used in the experimental animals, or injection of undamaged red blood cells.
人类婴儿高胆红素血症的主要促成因素之一是胆红素生成。通过估计内源性一氧化碳（CO）的生成量来间接测量胆红素生成速率，而一氧化碳是在血红素分解代谢过程中与胆红素以等摩尔量生成的，这一过程采用测定一氧化碳的肺排泄率的方法。目前尚无研究证实体内由已知量血红素分解代谢产生的CO通过肺排泄实现完全回收。我们在此报告了对五只成年雄性Wistar大鼠注射已知量的以在含有巯基抑制剂N - 乙基马来酰亚胺（NEM）的溶液中孵育而“受损”的红细胞形式存在的血红素后，一氧化碳肺排泄率的定量测定结果。以额外CO与血红素的摩尔比表示的高于基线生成量的“额外”CO的平均回收率为0.98±0.02（标准误）。对照研究表明，饥饿后、注射与实验动物所用剂量相当的NEM或注射未受损红细胞后均未产生额外的CO。
