Abstract
Abstract Sulfhemoglobinemia was produced in dogs and rabbits by administration of sulfur together with acetophenetidin, TNT, or p-aminopropiophenone. The sulfhemoglobin content of the blood, the unaltered hemoglobin, red cell, reticulocyte and white cell counts, serum bilirubin content, and bile pigment excretion were followed during the formation of the sulfhemoglobin and until its disappearance after the drugs were discontinued or after transfusion. In addition, cells containing sulfhemoglobin were followed by tagging with radioiron. Formation of sulfhemoglobin occurred most rapidly on administration of p-aminopropiophenone, least rapidly with acetophenetidin. All these drugs produced hemolysis at a rate apparently unrelated to sulfhemoglobin formation. Disappearance of sulfhemoglobin was due to a random destruction process as well as senescence of the cells containing it. There is no evidence for accelerated senescence. Quantitative estimation of sulfhemoglobin in blood is discussed, and new values are given for the specific extinction coefficients of reduced carboxyhemoglobin and CO-protohemochromogen.
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