Hypercholesterolemia, but not hypertriglyceridemia, was associated with increased platelet-dependent thrombin generation. Pravastatin normalized the generation of thrombin.

Coagulability is evidently enhanced in patients with non-insulin-dependent diabetes mellitus compared with that in healthy normal subjects on the basis of assessments of the platelet-dependent thrombin generation, and good glycemic control may help to correct a hypercoagulable state in diabetic patients.

Abstract. Erythropoietin is known to be effective for the treatment of anemia in chronic renal failure, but the efficacy of erythropoietin for anemia in other diseases is not so great. Insulin exerts a growth promoting activity in various kinds of cells. In the present study, the effects of insulin on erythroid progenitors (colony forming units-erythroid, CFU-E; and burst forming units-erythroid, BFU-E) in human bone marrow were examined at various concentrations of recombinant human erythropoietin (rh-Epo) to clarify the relationship between erythropoietin and insulin. Human insulin stimulated the formation of CFU-E and BFU-E in the presence of three concentrations (0.25, 5, and 100 Ulml) of rh-Epo. Stimulatory effects of human insulin on CFU-E and BFU-E were also observed in the nonphagocytic and nonadherent bone marrow fraction (NP-NA fraction) and in the NP-NA and T cell-depleted fraction at each concentration of rh-Epo. Human insulin further stimulated the CFU-E and BFU-E growth in CD34' separated bone marrow cells. These results indicate that the enhancing effect of human insulin on erythroid progenitors is not mediated through monocytes and macrophages or T cells, suggesting a direct action on erythroid progenitors.

No abstract

The purpose of this study was to angioscopically observe the process of thrombolysis after intracoronary administration of thrombolytic agents and to investigate the effects of these agents on coagulation/fibrinolysis systems in dogs. The coronary endothelium was removed and thrombus formation was confirmed by angioscopy. In the tissue plasminogen activator (tPA) group (n=8), complete thrombolysis occurred in all animals, but thrombolysis was incomplete in the urokinase (UK) group (n=6). The plasma level of plasmin alpha2-plasmin inhibitor complex peaked at 15 minutes after treatment in both the tPA and UK groups. Plasma thrombin-antithrombin III (TAT) complex decreased transiently at 15 minutes after tPA administration but increased at 30 and 60 minutes (P<0.05). In the UK group, plasma TAT also showed a transient decrease followed by an increase, which was minimal compared with that in the tPA group. Plasma TAT decreased transiently after infusion of tPA and subsequently increased to above the pretreatment level, suggesting a risk of rethrombosis after successful recanalization.