Abstract

<h2>Summary</h2> By the use of hemochromogenspectroscopy the substance giving positive benzidine and Nadi reactions in hyaline membrane has been identified as a hemoglobin-like compound. Proof of its iron content is further advanced by tinctorial demonstration of iron in most of the hyaline membrane found in the lungs of an adult case of mitral stenosis. From this it is argued that the development of pulmonary hemosiderosis in rheumatic mitral stenosis is on the basis of repeated episodes of hyaline membrane disease. It is reasoned that this heme in the membrane must come either from lysed extravasated red blood cells or from the mucosal epithelial cells of the respiratory bronchioles and alveolar ducts. Hemochromogen spectroscopy of other tissues has revealed hemoglobin-like compounds in sites other than red blood cells, viz., in the cells of the convoluted tubules of the kidney, ependyma of brain, and especially in the cells covering the chorionic villi of the placenta. It is pointed out that this layer frequently shows development of a condition not unlike hyaline membrane. These findings may mean that hemoglobin-like pigments are distributed throughout the cells of the body in proportion to their metabolic needs and may answer to the description of the "unspecific cell hematin"<sup>12</sup> of Keilin. A corollary of this work is that the Nadi reaction is not specific, at least in histological studies, for the cytochrome C and B compounds or for cytochrome oxidase, but that it is given catalytically by heme compounds in general. Also, diphenylthiocarbazone may be a useful stain for ferrous-porphyrins. Pilocarpine has been shown to enhancethe effect of oxygen in the genesis of hyaline membrane disease in experimental animals. Preliminary evidence is adduced to show that metabolic upset precedes the development of hyaline membranes, and work is now in progress to complete the picture of this metabolic upset.

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