Ultrastructural changes in the liver in heatstroke.

The ultrastructural changes in the human liver 24 to 96 hours after an attack of heatstroke are described. The alterations are most obvious along the vascular pole of the hepatocytes. These consist of degenerative changes or desquamation of sinusoidal lining cells, ballooning or flattening of microvilli, breaks in hepatocyte outer membranes, and electron-lucent vacuoles along the sinusoidal border. Also noteworthy is the appearance, in a number of cases, of basement membranes or ill-defined electron-dense material which may be of basement membrane character. Sinusoidal elements, such as erythrocytes, are found in hepatocytes, and hepatocellular debris appears in sinusoids. The membranes of hepatocytes and sinusoidal lining cells thus seem to be the prime targets of the hepatic injury in heatstroke. Other changes in the hepatocytes include vesiculation of endoplasmic reticulum, detachment of ribosomes, and alterations of mitochondria. Morphologic evidence of intravascular coagulation of intravascular hemolysis is often encountered. A comparison between the findings described here and those in experimental hyperthermia suggests that many of the hepatic changes seen in heatstroke are due to an excessively high tissue temperature per se but that some of the alterations are probably a consequence of complicating factors such as hypoxia, intravascular hemolysis, or disseminated intravascular coagulation.

Vitamin A-containing lipocytes and formation of type III collagen in liver injury.

Hepatocellular necrosis in carbon tetracholride-induced injury of rats is associated with an accumulation of lipocytes (perisinusoidal cells or Ito cells) containing fat droplets and giving vitamin A fluorescence. In the subsequent formation of connective tissue septa, transitional cells having morphologic characteristics of lipocytes and fibroblasts are abundant and are associated with the appearance of type III collage-. The features suggest that the lipocyte is the precursor of the fibroblasts responsible for parenchymal fibrillogenesis and under these conditions forms type III collagen. The process is a postulated link between hepatocellular necrosis and fibrosis.

Morphologic variants of alcoholic hyalin.

Liver biopsies obtained from 24 patients with alcoholic liver disease were studied by light and electron microscopy. Comparisons of the same cells in adjacent sections revealed that alcoholic hyalin is a fibrillar deposit without limiting membranes and is readily distinguished from giant mitochondria. This characteristic fibrillar structure was encountered in hepatocytes, ductular cells and in benign and malignant hepatomas. Three distinct morphologic forms of alcoholic hyalin were observed: a) bundles of filaments in parallel arrays, b) clusters of randomly oriented fibrils and c) a granular or amorphous substance containing only scattered remains of fibrils. Closely associated with alcoholic hyalin and often found along its entire circumference, were bundles of fine filaments in parallel arrangement of much smaller size. These occasionally displayed variations in orientation and merged with the filaments in the alcoholic hyalin body. Similar fine filaments were observed, in considerable excess, in cells which did not contain alcoholic hyalin. According to our findings, the fine filaments and the significantly larger filaments in alcoholic hyalin could be parts of a contractile system elaborated by host cells during the course of hepatic injury.