A comparison has been made between the prothrombin time test using British Comparative Thromboplastin (BCT) and a chromogenic substrate assay for factor VII in the assessment of laboratory control of oral anticoagulants in short-term and long-term patients. Opportunity was also taken to compare the findings with parallel results obtained with the venous Thrombotest technique and a specific clotting assay for factor VII. There was good agreement between the amidolytic factor VII assay, using a method modified from Seligsohn et al (1978) with the Quick test using BCT and Thrombotest in 60 long-term patients. Tests in 53 patients within the first 3 weeks of starting oral anticoagulant administration gave less satisfactory agreement between the above amidolytic method and the conventional tests. In contrast, there was a good correlation between the two conventional tests in both groups and also between the clotting and amidolytic factor VII method. Although the results are an improvement on previous, less satisfactory correlations between the BCT prothrombin time method and amidolytic assays for factor II and X, the present study indicates the limitations of a specific clotting assay versus a broad spectrum extrinsic clotting test in oral anticoagulant control. While not warranting the routine use of the chromogenic assay for factor VII in place of the prothrombin time using BCT, the factor VII amidolytic assay offers a limited but dependable guide to dosage in long-term patients. The complexity of the technique in its present form militates against its adoption for routine anticoagulant control in hospital laboratories.
Studies have been undertaken to compare amniotic fluid from patients with pre-eclampsia (PET) with normotensive controls in inhibiting platelet aggregation (PGI2-like activity) and accelerating coagulation tests. After 39 weeks of gestation, samples from PET patients showed significantly less PGI2-like activity (p<0.001) and significantly lower kallikrein levels (p<0.01) than normotensive controls. These findings suggest that the biosynthesis and release of these substances may be impaired in PET. In view of the association of PET with intravascular clotting, the highly significant reduction of PGI2-like activity appears important and warrants a clinical trial of prostacyclin administration in this disorder.
In 1981, a new low-molecular-weight protease inhibitor, FUT-175 (nafamstat mesilate), was synthesized. Its preventive action against acute experimental pancreatitis (AEP) was detected. We studied the effect of FUT-175 on the blood count and aggregability of platelets in AEP in dogs. At 30 min after induction of AEP, the sensitivity to ADP increased more than two times in untreated animals. An evident decrease in platelet count of about 37% was noted in these dogs at 6h after AEP induction. Treatment of AEP with FUT-175 prevented these changes. We assume that the positive effect of FUT-175 against AEP depends at least in part on its influence on platelet aggregation.
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