No abstract

An electron microscopic study of the tibial epiphyseal plates of growing rats reveals that the resorption of unmineralized and mineralized cartilage occurs by two different mechanisms. During resorption the unmineralized transverse cartilaginous walls between chondrocytes are invaded by capillary sprouts. At the resorption zone, numerous cytoplasmic processes derived primarily from the perivascular cells and, to a lesser extent, from the endothelial cells of the sprouts penetrate and appear to lyse the unmineralized transverse cartilaginous walls. Hydrolases released from the degenerating chondrocytes and/or capillary sprouts may also participate in this process. The second resorption mechanism involves the mineralized longitudinal cartilaginous septa. Resorption of these septa is mediated by chondroclasts whose fine structure is identical with that of osteoclasts. The active surface of the chondroclasts has a ruffled border. The surface membrane of the chondroclasts is relatively smooth on either side of the ruffled border and lies in direct apposition with the underlying mineralized cartilage. This observation suggests that the microenvironment in the zone of resorption may be maintained by the neighboring unruffled surfaces of the chondroclasts, which thus seal off and segregate the active portions of these cells.

l~otraE 8 This electron micrograph presents the septate junction. Regularly spaced septa, which bridge the intercellular space, are present. X 60,000. The inset is similar. X 78,000.

No abstract

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.