By J. De Groote (auth.), P. Fondu MD, O. Thijs MD (eds.)

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I would be very surprised if that sort of cell specifically in the liver would produce FVIII:c. For other physiological reasons, for example the release of FVIII:c when you give DDAVP, which is so instantanious and so potent that I would be very surprised if it attacks that target side like that in the liver. But I think that remains to be seen. Vinnazer You don't have normal levels of coagulation factors in rats so how did you make you calibration curve? Giddings Yes, we did not have a reference material, we did not have a reference standards in rats; what we did, was to pool a lot of rat plasma and to use that to relate to humans.

Synthesis of V and VIlle was inhibited by actinomycin and cycloheximide in a manner similar to that observed with factors II, IX and X and was not inhibited by Warfarin. The cells which synthesise V and VIlle are susceptable to ethionine and indian ink suggesting possible reticulo-endothelial cell origins. Relatively more VIlle than VlllRAg was synthesised in the isolated liver perfusion system and exogenous VIllRAg was consistently removed from the circulating perfusate. In spite of extensive efforts the precise cellular sites of synthesis of V and VIlle remains to be established.

We were unhappy about calling it a quantitated value in the assay; simply we have just shorten the clotting time. But we were getting calibration curves with normal pooled rat plasma. 24 ORAL ANTICOAGULANTS: UNEXPECTED SIDE-EFFECTS OR NEW FIELDS 'OF APPLICATION? G. D. BERG, M. M. SOUTE, MENNO DE METZ AND CEES VERMEER* 1. SUMMARY Vitamin K-dependent carboxylase is found in liver and in a number of non-hepatic tissues vessel wall. partial such as: It is shown, inhibition of the testis, lung, kidney, spleen and that the dosages of warfarin, clotting factor synthesis arterial required for a also affects the non-hepatic vitamin K-dependent systems.

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