Abstract
With prolonged exposure to a soln. of lead acetate, definite evidence of absorption of lead was obtained. The surface mucus did not constitute an efficient barrier to the entrance of the metal as Carpenter (see B. A. 3 entry 13083 and 7: entry 8488) found in more acute exps. with fishes. The degree of destruction of the erythrocytes was used as a measure of the rate of the absorption of lead. An early mild regenerative response occurred, but eventually a pronounced secondary anemia was produced. Little phagocytosis of dead cells occurred in the peripheral circulation, but the pigment derived from dead red cells was progressively stored in the interstitial tissues of the liver, spleen and mesonephros. The hepatic cells also became crowded with pigment granules. No storage was observed in the heart. The pigment was accumulated chiefly in macrophages of local origin which, after ingesting erythrocytes, desquamated and migrated into the connective tissues. Monocytes and eosinophiles were increased slightly in number in the blood stream, but the most striking change occurred in the nos. of atypical thrombocytes, and spindle cells which may belong to the thrombocytic series. The endothelium of the heart showed marked proliferative activity; in some regions there was localized differentiation of erythrocytes; in other regions the atypical elongated cells, just referred to, were formed in large radiating clusters on the surface of the ventricular trabeculae. No explanation of the latter response to lead poisoning can be given.