Batroxobin, in combination with low molecular weight heparin for the treatment of progressive stroke: clinical observations. The key to this approach is reducing blood viscosity and platelet aggregation in acute cerebral infarction, increasing blood fibrinolytic activity, promoting arterial thrombolysis, and providing antithrombotic thrombolytic therapy to prevent the expansion of the infarct and perivascular thrombosis formation.
Batroxobin decomposes fibrinogen into fibrin monomer, thereby effectively reducing the concentration of plasma fibrinogen to prevent platelet thrombosis. It also induces vascular endothelial cells to release tissue-type plasminogen activator, converting plasminogen into plasmin, thus exerting an antithrombotic effect.
Low molecular weight heparin has a much longer biological half-life than regular heparin, possesses fibrinolytic properties, enhances the anticoagulant effect of vascular endothelial cells, and reduces blood coagulation. Its anti-Xa activity effectively prevents the ischemic progression of stroke with fewer side effects and no obvious bleeding tendency.
It can be seen that the combination of Batroxobin and low molecular weight heparin in the treatment of progressive stroke demonstrates clinical efficacy. Prothrombin time, fibrinogen levels, and platelet counts were better in the treatment group compared to the control group, and no cases of hemorrhagic cerebral infarction were found in either group.
In short, the combination of batroxobin and low molecular weight heparin for the treatment of stroke not only improves efficacy but also minimizes side effects.