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The response of mononuclear phagocytes to three inert particles--barium sulfate, talc, and thorium dioxide--was studied by correlated light and electron microscopy. All three particles induced maturation of the mononuclear phagocytes, which proceeded to the stage of the mature macrophage and required 7 to 9 days. Once established, maturation persisted as long as 45 days, as did the inert particles. The resultant lesions, dense aggregates of mature macrophages, were termed mature granulomas. The resultant maturation differed from that produced by digestible bacteria in tempo and extent but not in pattern.

Right ventricular papillary muscles from control cats and from cats subjected to hemorrhagic shock were studied by electron microscopy. Half of the muscles were fixed at the apex of their active length-tension curves following stimulation in a papillary muscle bath. The other half were also fixed under tension. The ultrastructure of each muscle was examined in detail. A series of stages in the formation of myocardial zonal lesions, ranging from minimal changes in the intercalated discs to severe lesions, were identified and interpreted as representing the sequential stages in the formation of zonal lesions. One of the earliest (least severe) changes in the formation of zonal lesions, the separations of actin filaments from the intercalated disc, may be critical to the subsequent development of cardiac failure in hypovolemic shock. Mitochondrial displacement was a late event in the formation of the lesions, occurring only after major alterations had taken place in the sarcomeres and intercalated discs. It was noted that the ultrastructure of mitochondria remained essentially normal, and that there was no cell swelling associated with zonal lesions. This serves as confirmatory evidence that myocardial zonal lesions are a unique form of myocyte injury, are potentially reversible, and are not caused by ischemia.