Publisher Summary This chapter discusses preparation of isolated rat liver cells The early mechanical and chemical methods for liver-cell preparation were relatively successful in converting liver tissue to a suspension of isolated cells The successful preparation of intact liver cells by perfusion with collagenase is technically quite difficult The major method for preparation of nonparenchymal liver cells is based on the selective sensitivity of parenchymal cells toward proteases By incubation of rat liver minces with pronase, most of the liver parenchyma is digested, while nonparenchymal cells remain intact and can be recovered from the incubate Similar results have been reported with trypsin digestion of collagenase-dispersed liver minces, but pronase appears to be more effective The most common procedure is to perfuse the liver briefly with pronase before it is minced and incubated with the enzyme Such direct pronase methods have been used by several investigators with yields of nonparenchymal liver cells reported to be in the range 2–15 × 10 6 cells/gm liver

Preparation of isolated rat liver cells.

Epidermal growth factor-related peptides and their receptors in human malignancies

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.24452

Diagnostic accuracy and reliability of ultrasonography for the detection of fatty liver: A meta‐analysis

Primary culture of parenchymal liver cells on collagen membranes. Morphological and biochemical observations.

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.1840200227

Inactivation of Kupffer cells prevents early alcohol-induced liver injury.

https://www.gastrojournal.org/article/0016-5085(90)90967-6/pdf

Provocation of massive hepatic necrosis by endotoxin after partial hepatectomy in rats

Serum hepatocyte growth factor levels in hepatectomized and nonhepatectomized surgical patients

Rats received a dose of dimethylnitrosamine (DMN) or carbon tetrachloride (CCl4). In the liver of rats given DMN, apoptosis of fat-storing cells occurred at 7.5 h, and sinusoidal endothelial cell degeneration followed, with parenchymal cell necrosis after 9 h. Fibrin thrombi appeared in the sinusoids as well as in these necrotic areas after 12 h. In contrast, in the liver of rats given CCl4, parenchymal cell degeneration was seen after 6 h and necrosis with fibrin thrombi developed after 9 h. Fat-storing cells and endothelial cells were almost intact, and fibrin thrombi were not present in the sinusoids. SGPT values increased with decreased plasma levels of fibrinogen and antithrombin III and prolonged prothrombin time after 3 and 6 h, in the CCl4 and DMN models, respectively. An extensive reduction in plasma factor VIIIC levels and peripheral platelets was seen after 18 and 24 h, respectively, only in the DMN model. These results suggest that endothelial cells destruction can cause fibrin formation in the hepatic sinusoids in acute liver injury. Fat-storing cell injury may contribute to the destruction.

Hepatic sinusoidal cell destruction in the development of intravascular coagulation in acute liver failure of rats.

https://www.gastrojournal.org/article/0016-5085(93)90357-I/pdf

Sinusoidal endothelial cell damage by activated macrophages in rat liver necrosis

Liver damage was induced in rats by injection of dimethylnitrosamine (DMN) or carbon tetrachloride (CCl4). Fibrin clots were observed in the hepatic sinusoids at 12 hours and soluble fibrin monomer complexes were markedly detected at 24 hours only in the rats given DMN. When antithrombin III concentrate was infused at 12 hours there was a dose dependent improvement of the values of serum total bilirubin, SGPT, prothrombin time, peripheral platelet count, and plasma fibrinogen and coagulation factor VIIIC and of the histological degree of liver injury at 24 hours in the DMN group. The CCl4-group showed no such improvement. Intravascular coagulation may complicate the course of certain types of acute liver injury and contribute to its aggravation in rats. Under such circumstances, treatment with antithrombin III concentrate would be beneficial.

https://gut.bmj.com/content/gutjnl/29/8/1103.full.pdf

Kenji Fujiwara

Papers

Provocation of massive hepatic necrosis by endotoxin after partial hepatectomy in rats

Serum hepatocyte growth factor levels in hepatectomized and nonhepatectomized surgical patients

Hepatic sinusoidal cell destruction in the development of intravascular coagulation in acute liver failure of rats.

Sinusoidal endothelial cell damage by activated macrophages in rat liver necrosis

Intravascular coagulation in acute liver failure in rats and its treatment with antithrombin III.