Susumu Oshiba

Hormonal regulation of plasminogen activator production by rat hepatocytes in primary culture.

Hormonal regulation in the production of a plasminogen activator (PA) was studied in rat hepatocytes in primary culture. Insulin and epidermal growth factor had no effect on the hepatic PA activity. However, glucagon and epinephrine augmented the activity, whereas dexamethasone suppressed it by lowering the production of hepatic PA rather than by inducing plasmin inhibitors or a plasminogen activator inhibitor (PAI). Dibutyryl cAMP, an analogue of cAMP, also augmented hepatic PA activity. The augmented activity level was lowered by either H-8, cycloheximide, or actinomycin D, suggesting that A-kinase and protein biosynthesis are closely associated with the augmentation. Glucocorticoid and hormones that act to raise the intracellular cAMP level may participate in hepatic PA production by the liver.

Studies on bilokinase, a biliary plasminogen activator: Immunologic property and organ distribution

The aim of the present study was to elucidate the immunologic difference between bilokinase, a plasminogen activator in bile, and urokinase, an urinary plasminogen activator, and to demonstrate the organ distribution of these antigens. Polyclonal antibodies against the highly purified activators (bovine-bilokinase, -urokinase and human urokinase) were raised in rabbits or guinea pigs. Immunologic precipitin reactions and quenching were found to occur only between the activators and their respective antisera. Histo-immunologic demonstration of the activators revealed that bilokinase-antigen was localized mainly in the hepatocytes as well as in the mucosa of the gall bladder, whereas urokinase-antigen was present in the epithelium of the urinary tubules. The liver may have a potential role in the hepatobiliary fibrinolytic system.

Cysteamine-induced duodenal ulcer and the hepatoduodenal branch of the vagus nerve

SummaryWe investigated the role of the autonomic nervous system in gastric acid secretion, somatostatin concentration and PAS-positive mucus production in Brunner’s glands in cysteamine-induced duodenal ulcer. Vagotomized rats were used. No ulcers occurred in the groups with vagotomies of the hepatoduodenal, truncal or gastric branches after cysteamine administration. However, in the hepatoduodenal branch vagotomized group, there was an increases in gastric acid secretion after cysteamine administration. A similar increase was observed in the control group, but the decreases in somatostatin concentration and PAS-positive mucus seen in the control group were not found in the hepatoduodenal vagotomized group. These results suggest that the hepatoduodenal branch of the vagus nerve might play an important role in the ulcerogenic process of cysteamine-induced duodenal ulcer.

Turnover of fibrinopeptide A (FPA) in rabbits

FPA disappeared from the circulating blood along a double-exponential decay curve consisting of an initial phase (t 1/2 = 1.8 min) and a late phase (t 1/2 = 34.7 min). The rapid decrease in blood FPA was due to the large extravascular space, the size of which was estimated to be about 5 times larger than that of intravascular space. The actual amounts of 125I-FPA distributed to the organs and tissues were generally quite low. However, in the case of the urine, the injected amount of FPA was excreted at the rate of 50% per hour. Thus, the urinary FPA levels may reflect the occurrence of intravascular coagulation.