Initiation and recovery processes of endotoxin induced disseminated intravascular coagulation (DIC): scanning and transmission electron microscopic observations of rat renal tissues.

To clarify the initiation, development and recovery processes of disseminated intravascular coagulation (DIC), rat glomerular capillaries and fibrin thrombi were examined under transmission and scanning electron microscopes. DIC was induced in rats by a single intraperitoneal injection of endotoxin (Et., 7.5 mg/kg lipopolysaccharide:B, E. coli 026:B6). At 2 h after Et. injection, the endothelial surface of the glomerular capillary became irregular with projections like a sea anemone. At 4 h after Et. injection, agglomerated fibrin thrombi composed of fibrin fiber bundles with fine cross-striated fibriform structures were observed in the capillary lumen. The fibrin thrombi gradually changed into fine reticular systems suggesting a degradation process by 6 h after Et. injection, and formed a coarse granular agglomerate by 8 h after Et. injection. These fibrin thrombi disappeared within 12 h of Et. injection, but the endothelial surface remained edematous. At 24 h after Et. injection, the microstructure of the glomerular capillaries returned normal. Based on these observations, we concluded that DIC was primarily initiated by injury to the capillary endothelium, and that changes on the endothelial surface contributed to the development of DIC.</p

Importance of immunoenzyme histochemical reaction in diagnosis of disseminated intravascular coagulation in human and animal material.

Renal tissues from 208 human necropsies were observed histologically for disseminated intravascular coagulation (DIC). The tissues were stained with hematoxylin-eosin, Mallory's phosphotungstic acid hematoxylin (PTAH) and cationic ferric hydroxide colloid stabilized with cacodylate (Fe-Cac), and tested by immunoenzyme histochemical (IEH) reaction for fibrin-related materials (FRMs). The use of the IEH method increased FRM recognition, and FRMs were detected in a total of 80 cases (38.5%). In 26 cases diagnosed clinically as DIC, FRMs were shown in 23 of the cases (88.5%). Thus, 57 patients with FRMs were clinically asymptomatic. In rats with DIC induced by endotoxin injection, glomerulus FRM was effluxed into the tubulus through the Bowman's capsule and was excreted into urine. The electric charge was reduced on the endothelial surface of the glomerular capillaries in both human and rat DIC. Under the scanning electron microscopy, the endothelial surface appeared coarse in the glomerular capillary and fibrin degradation was present. Our conclusions are: (a) PTAH is non-specific for FRMs, (b) IEH aids the pathohistological diagnosis of DIC, especially in asymptomatic forms including the compensated DIC state, (c) FRMs in tubuli suggest DIC, and (d) DIC is possibly initiated by a reduction in the capillary electric surface charge.</p

A case of necrosis of hepatocellular carcinoma and tumor thrombus in the portal vein induced by transcatheter arterial lipiodol chemoembolization.

A case of hepatocellular carcinoma is reported in which the main tumor, intrahepatic metastases and a tumor thrombus in the portal vein were necrotized completely after Lipiodol chemoembolization. In this case, the tumor thrombus seemed to act as a portal embolus. This phenomenon is interesting because Lipiodol chemoembolization alone usually can not necrotize intra- or extra-capsular invasion, intrahepatic metastasis or tumor thrombus in the portal vein. This case is considered to be suggestive of a possible therapy for hepatocellular carcinoma.</p