Effects of tranexamic acid, cis-AMCHA, and 6-aminohexanoic acid on the activation rate of plasminogen by urokinase in the presence of clot.
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Biomedical subjects
Publications and source records attributed to A Takada.
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The relationships between the haemolytic activities of complement and its components were studied. The activities studied included CH50 (classical pathway), AP50 (alternative pathway), CV50 (early part of alternative pathway) and C(3--9)H50 ((the late part of both pathways). The components included C3, C4, C5, C9, B and D. There was a good correlation between CH50 and AP50. AP50 had a good correlation with B and CV50. There was no correlation between AP50 and C(3--9)H50, and none between C(3--9)H50 and C5 or C9. AP50 may primarily represent changes in the early part of the alternative pathway. C(3--9)H50 is not influenced by respective changes in the amounts of C5 or C9. Since cell lesion is now considered to be caused by a unit of C5b to C9, a change in each component of C5 to C9 may not influence haemolytic activity.
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The esterase activity of highly purified human urokinase on Nalpha-acetylglycl-L-lysine methyl ester is strongly inhibited by 1 X 10(-5) to 1 X 10(-2)M Cu++, Hg++, Ni++, Co++, Fe+++, and Mn++ solutions, whereas Na+, K+, Ca++, and Mg++ are weakly effective. This inhibition is parallel with the inhibition of activation of plasminogenby urokinase. There is no simple linear relation between inhibiton and concentration. Addition of ethylenediaminetetraacetate or electrodialysis fully reactivates the inhibited enzyme. These results are discussed in relation to similar effects of ions on trypsin.
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The color reaction of cholesterol with trichloracetic acid and antimony trichloride was examined to elucidate its reaction mechanism. 3,5-Cholestadiene, 3,3'bis(3,5-cholestadiene), 3,3'bis(2,4-cholestadiene), and cholesteryl trichloroacetate were isolated as the reaction products from the colored reaction mixture of cholesterol, and the first three compounds were found to be responsible for the coloration. It was assumed that cholesterol was dehydrated to 3,5-cholestadiene and 2,4-cholestadiene, which were dimerized to 3,3'-bis(3,5-cholestadiene) and 3,3'-bis(2,4-cholestadiene), respectively, and 3,3'-bis(2,4-cholestadiene) was in part converted to 3,3'-bis(3,5-cholestadiene) in trichloroacetic acid and antimony trichloride. The free radicals were detected in the colored solutions of choelsterol, 3,5-cholestadiene, 3,3'-bis(3,5-cholestadiene), and 3,3'-bis(2,4-cholestadiene), and inferred to be the radical cations of the steroids. The radical cation was postulated to be responsible with respect to the mechanism of the coloration. The relationship between the color reagent and the formation of dimeric steroids was described.
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Effects of various aminoacids and their derivatives on the classical pathway and alternative pathway of the complement were studied. Leupeptin, acetyl-leucyl-leucyl-arginal, inhibited CH50 and Cl-esterase, but did not inhibit the alternative pathway. When aminoacids of carbon chains of the order of seven were used, arginine and lysine had stronger effects than trans-aminomethyl cyclohexane carboxylic acid (t-AMCHA), cis-aminomethyl cyclohexane carboxylic acid (cis-AMCHA) and epsilon aminocaproic acid (EACA). SH-compounds, cysteine, homocysteine and glutathione, had the strongest inhibitory effects among these aminoacids on both classical and alternative pathways. When effects on Cl esterase were compared, arginine, lysine, t-AMCHA, cis-AMCHA and EACA had weak inhibition while SH-compounds showed strong inhibition. Poly-L-lysine, which had extremely strong inhibition of CH50, had no inhibition of Cl esterase. The inhibitory effects of antifibrinolytic agents, EACA and t-AMCHA, were weak but when effects on early parts of the classical pathway, C(1,4,2)H50 were tested, some inhibitory activities were recognized. Thus inhibitory effects of these agents were due to their activities on the early parts of the classical pathway.
An attempt was made to find reliable indices for the early recognition of fatal cases of acute viral hepatitis, using the values of serum proteins with rapid turnover. Prealbumin and alpha2-HS-glycoprotein were measured in the sera of 44 cases by immunodiffusion method before the appearance of hepatic coma and/or gastrointestinal bleeding. The difference of the mean values of prealbumin between fatal and surviving cases of subacute form of fulminant hepatitis was not statistically significant. In contrast to this, there was statistically significant difference between both groups in the mean values of alpha2-HS-glycoprotein (p less than 0.05). The present results indicate the possibility of differentiating fatal cases from surviving ones at an early stage, using the reduction of alpha2-HS-glycoprotein by a simple and reproducible immunodiffusion method.
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