ENDOGENOUS CARBON MONOXIDE PRODUCTION IN PATIENTS WITH HEMOLYTIC ANEMIA
ENDOGENOUS CARBON MONOXIDE PRODUCTION IN PATIENTS WITH HEMOLYTIC ANEMIA
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DOI：
10.1172/jci105360
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发表时间：
1966-01-01
影响因子：
15.9
通讯作者：
KAHN, SB
中科院分区：
文献类型：
--
作者：
COBURN, RF;WILLIAMS, WJ;KAHN, SB
本文研究了7例溶血性贫血患者内源性一氧化碳生成与红细胞和血红蛋白分解代谢的关系。所有患者的CO生成率均显著升高，并与放射性铬酸盐红细胞标记研究计算的血血红素破坏率密切相关（r = + 0.94）。在8项研究中，有6项研究产生了比血液血红素分解代谢所能解释的更多的一氧化碳。平均摩尔比为1。[加减]0。28 (SD)。一氧化碳的部分显然不能根据循环血红蛋白分解代谢来解释，“额外的一氧化碳”可能是代谢过程的副产品，导致“分流”胆色素。红细胞的平均寿命可以根据CO的产生率计算，校正额外的CO，误差为[正负]3天（SD）。
The relationship of endogenous CO production to red blood cell and hemoglobin catabolism in 7 patients with hemolytic anemia was investigated. The rate of CO production was markedly elevated in all of the patients and correlated closely with the rate of blood heme destruction calculated from radio-chromate red blood cell labeling studies (r = + 0.94). Greater amounts of CO were produced in 6 of 8 studies than could be explained on the basis of blood heme catabolism. The average molar ratio was 1. 41 [plus or minus] 0. 28 (SD). The fraction of CO apparently not explainable on the basis of circulating hemoglobin catabolism, "extra CO, " may be a by-product of the metabolic processes that cause "shunt" bile pigment. Mean erythrocyte life-spans can be calculated from the rate of CO production corrected for extra CO with an error of [plus or minus] 3 days (SD).