Two active compounds that prevent serotonin-induced ulcerogenesis in rats were isolated from Chinese cinnamon (the stem bark of Cinnamomum cassia) and identified as 3-(2-hydroxyphenyl)-propanoic acid and its O-glucoside. The former compound, administered orally or parenterally to rats at a remarkably low dose (40 micrograms/kg body weight), also inhibited gastric ulcers induced by the other ulcerogens such as phenylbutazone, ethanol, and water immersion stress, although it failed to prevent indomethacin-induced ulcers. Pharmacological studies have shown that 3-(2-hydroxyphenyl)-propanoic acid hardly inhibited the secretion of gastric acid, but promoted the gastric blood flow. These results suggest that the antiulcerogenic effect of this compound is probably attributable to the potentiation of defensive factors through the improvement of the circulatory disorder and gastric cytoprotection.

The effects of portal, hepatic arterial and femoral venous administration of prostaglandin E1 (PGE) on portal venous flow (PVF) and hepatic arterial flow HAF were examined before and after 70% hepatectomy in anesthetized dogs. In the hepatectomized condition, portal venous administration of PGE (0.5 microgram/kg/min) caused an increase in PVF without any change in systemic arterial pressure (SAP). HAF was unchanged following the injection. The portal effect of PGE on PVF was dose-dependent, and a reduction in portal venous resistance was seen. However, the same dose of PGE failed to change PVF under intact liver conditions. Hepatic arterial administration of PGE (0.5 microgram/kg/min) brought no significant change in PVF or HAF, with or without hepatectomy. Femoral venous administration of PGE (0.5 micrograms/kg/min) produced an increase in PVF concomitant with a significant decrease in SAP. HAF showed no change after the injection. A decrease in PVR was seen only in the hepatectomized condition. It is concluded that PGE is potent in increasing PVF in the hepatectomized condition, and the portal vasculature is involved as the site of action.

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The specificity, distribution and rate of uptake of radiolabelled ¹²⁵I-Lys-plasminogen by in vitro thrombi was investigated. ¹²⁵I-Lys-plasminogen was added to whole blood perfusion mediums containing preformed thrombi and to whole blood prior to thrombus formation. Uptake was assessed by means of radioisotopic analysis and autoradiography. The plasminogen was taken up by thrombi during and after their formation. The largest percentage was in the fibrin component. ε-Aminocaproic acid-blocking experiments confirmed the specificity of plasminogen binding to fibrin. Autoradiography of the thrombi revealed plasminogen in the RBC-fibrin part and in platelet-fibrin aggregates. Plasminogen uptake and penetration into preformed thrombi were found to increase as a function of time. However, formation of thrombi from plasminogen-enriched blood was a more effective means for increasing the plasminogen content of thrombi than perfusion of preformed thrombi in a plasminogen-enriched medium, over the time period studied.