Edema from intracerebral hemorrhage: the role of thrombin

TLDR

The mechanism by which intracerebral hemorrhage causes brain edema remains unclear. The study aims to determine whether specific blood components are toxic to surrounding brain tissue. Rats received stereotactic infusions of various solutions into the right basal ganglia, and after 24 hours brain edema and ion concentrations were measured. Whole blood induced brain edema and ion shifts, whereas isolated blood cells, serum, or plasma did not; however, activating coagulation with prothrombinase or inhibiting thrombin with hirudin modulated the edema, indicating thrombin’s key role in hemorrhage‑induced brain swelling.

Abstract

✓ The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.