Joseph Wiener

Electron Microscopic Alterations at the Alveolar Level in Pulmonary Edema

The electron microscopic alterations of the alveolar septum in advanced hemodynamin and alloxan-induced pulmonary edema were compared. Pulmonary edema was produced in anesthetized dogs by means of increased lefy atrial pressure and hemodilution and by allocan administration. Sections of pulmonary tissue from these dogs and similarly anesthetized controls were processed for and examined by light and electron microscopy. In the hemodynamic form of edema the interstitial fluid collects only in the collagen-containing portions of the septum. The endothelium, epithelium, their respective basement membranes and large portions of the air-blood barrier are unaffected. Alloxaninduced edema, in contrast, is characterized by degeneration of both endothelium and epithelium and by the appearance of fibrin within the alveoli. The hemodynamic type of pulmonary edema appears to result from an accentuation of the normal process of fluid exchange within the lung. Allocan-induced edema, on the other hand, is a pathologic process. The functional implications of these results are discussed.

Electron microscope studies in experimental thrombosis

Abstract Thrombi were produced experimentally in rats and studied at various stages of organization with the electron microscope. Fibrin, which is a prominent constituent of the early thrombus, was virtually absent after 4 days. There was evidence of collagen formation within the wall at 2 days, and there was extensive fibrogenesis within the thrombus at 4 days. The thrombi were first recanalized by solid cell cylinders which were converted into mature capillaries by a process of growth and fusion of extracellular spaces between adjacent endothelial cells. Other significant features and problems relating to the organization of thrombi are briefly discussed.

Fine Structural Aspects of Reticuloendothelial Blockade

Aschoff first introduced the term “reticuloendothelial system (RES)” to designate cells with marked ability to take up dyes [1]. Much literature has accumulated since the early studies pertaining to the incorporation of both particulate and soluble materials by the cells of the RES. The subject of RES blockade has also attracted considerable attention. The following mechanisms have been proposed for blockade: (1) Saturation of phagocytic cells [2], (2) Clones of phagocytic cells [3] with one substance preventing further phagocytic activities, (3) the blockading agent damages the phagocytic cells [4–6], (4) RES blockade results from the depletion of serum opsonins [7–8] or other serum factors [9] that are essential for the phagocytic process.