The study was made of the antibacterial effects of three terpene alcohols on Staphylococcus aureus, focusing on the leakage of K+ ions and toxicity over time. The leakage of K+ ions was monitored continuously with a K+-electrode. Our results suggested that the terpene alcohols, namely, farnesol, nerolidol and plaunotol might act on cell membranes. The rank order of effectiveness, farnesol>nerolidol>plaunotol, was the same in the toxicity assay and in the examination of the leakage of K+ ions, when we considered the initial rate and the amount of leaked K+ ions. The rank order agreed with the results of a growth-inhibition assay reported previously. The antibacterial activity reflected the initial rate of leakage of K+ ions, suggesting that damage to cell membranes might be one of the major modes of action of these terpene alcohols. The results also demonstrated that the initial rate of leakage and the amount of leaked K+ ions are useful as indices of the antibacterial activities of hydrophobic compounds.

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Disseminated intravascular coagulation (DIC) or renal damage associated with septicemia was induced in rats by ligating the cecum or by injecting endotoxin. In the septicemia model, the number of E. coli and Bacteroides spp in the blood increased concomitantly with an increase of endotoxin. In this model the development of hypercoagulability with mild fibrinolysis was observed. Histopathologic findings in the kidneys, including the formation of microthrombi in the glomeruli and the vacuolization and dilatation of renal tubular cells, suggest the development of mild DIC. In the endotoxin-induced DIC model, both remarkable state of hypercoagulability and fibrinolysis were observed with fibrin thrombi in glomeruli. The administration of the platelet-activating factor antagonist, CV-6209, or of human antithrombin III, ameliorated DIC significantly by limiting the increases in prothrombin time, activated partial thromboplastin time and fibrin degradation products. These agents significantly reduced the deposition of fibrin in the glomeruli and significantly prolonged the survival time of the endotoxin injected rats. These observations suggest that the PAF antagonist CV-6209 and ATIII merit clinical evaluation in the management of DIC caused by septicemia.antithrombin III (ATIII) ; endotoxin ; CV-6209; DIC ; septicemia Because of the development of chemotherapy, the treatment for infectious disease is not difficult in general. However, such complications as disseminated intravascular coagulation (DIC) or multiple organ failure (MOF) followed by septicemia is still refractory and shows a high mortality rate. MOF could be induced by septic shock or DIC with endotoxemia. The endotoxin seems to affect both the intrinsic and extrinsic pathways (Osterud and Bjorklid 1982;Rietschel et al. 1982;Colucci et al. 1983). The endotoxin activates factor XII directly (Morrison and Cochrane 1974) and stimulates the generation of the tissue factor from the monocytes and endothelial cells (Osterud and Bjorklid 1982;Colucci et

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