Pathways to Blood Coagulation Product I Formation

The basic reagent used was an eluate obtained from barium sulfate usedto adsorb various sera. When this eluate was prepared from normal rabbitserum, it responded to treatment with coagulants from adsorbed plasma,with Stypven, or with 25 per cent sodium citrate to give products withsimilar if not identical properties. With each preparation a stable complexformed with cephalin which withstood washing, was relatively heat-stable,was inactivated by adsorbed serum, and which required factor V for optimalprothrombin conversion. In eluates prepared from human serum, normalactivation occurred in the absence of factor IX, but was defective in theabsence of factor X. A preparation of factor X purified by DEAE cellulosechromatography was activated by 25 per cent sodium citrate. It is suggestedthat product I, the product of Stypven activation, and autoprothrombin Crepresent similar or identical reagents; it is further suggested that factor Xis their common precursor.

Submitted on November 7, 1962 Accepted on January 23, 1963     

Precipitous Rise and Fall of SGOT

Three patients are reported whose studies showed a transient but marked elevation of serum transaminase levels with a rapid return toward normal. In two patients this phenomenon was associated with transient episode of hypotension; in the third case this was an incidental finding discovered fortuitously on a routine test. Hepatic ischemia and parenchymal injury may cause transient elevations of serum transaminase levels.     

Effects of aspirin,indomethacin, flufenamic acid and paracetamol on prostaglandin output from rat stomach and renal papilla in-vitro and ex-vivo

The effects of aspirin, indomethacin, flufenamic acid and paracetamol on prostaglandin (PG) biosynthesis were studied in whole cell preparations of rat renal papilla and stomach in-vitro and ex-vivo. In the ex-vivo experiments a low dose aspirin was a potent inhibitor of PGE output from the stomach but not the renal papilla, while in-vitro renal PGE output was inhibited by aspirin to a greater extent than gastric PGE. Indomethacin and flufenamic acid inhibited both renal papillary and gastric PGE outputs in-vitro and ex-vivo. Paracetamol enhanced PGE output from the stomach more than twice ex-vivo, and to a lesser extent in-vitro. It also augmented PGE output from the papilla ex-vivo but not in-vitro. In view of the possible contribution of cellular organization and pharmacokinetic processes to the ultimate effect, it is suggested that studies on the effects of anti-inflammatory and antipyretic agents on PG biosynthesis should not be restricted to fully in-vitro systems.