Role Of Thrombin And Blood Products

Blood and blood products seem to consistently produce severe histologic injury, as compared to other inert substances, when injected into brain (17,18). The infusion of packed red blood cells into the cerebral parenchyma produced brain edema in 3 days. Likewise, when lysed blood was injected into brain, edema developed in 24 hr, which is consistent with the hypothesis that some factor within the red blood cell is responsible for causing the edema produced with whole blood injection (16). In addition, injection of intact or lysed red blood cells increases BBB permeability, contributing to edema formation (62).

When thrombin has been reported to cross the damaged BBB it has been associated with the development of inflammation, and perihematoma edema (19,63-65). Thrombin also causes less intense disruption of the BBB, as compared to lysed red blood cells (66). Experimentally depleting cells involved in inflammation, such as leukocytes and platelets, has been shown to ameliorate the extent of ICH-induced brain injury in animal models (67).

Thrombin has also been implicated in apoptosis. In an animal model, when thrombin was injected in brain, the peak to apoptosis preceded the peak that was induced by the injection of autologous blood (68). Apoptosis involves single cells and results in programmed cell death, with subsequent phagocytosis by adjacent normal cells (69,70). Apoptosis has been implicated in ICH in experimental models, persisting for up to 72 hr after the onset of the hemorrhage (71,72), and it has recently been found to be a common feature in ICH in humans, occurring as early as 24 hr after ICH onset. No relationship was found between severity of apoptosis, age, initial Glasgow Coma Scale, hematoma volume, and time between onset and hematoma evacuation. Interestingly, apoptosis was not observed in specimens from cerebel-lar hematomas, which may reflect differences in cell populations and the spatial distributions of neurons (73).

These observations suggest that apoptotic processes occur in an ongoing delayed manner and are potentially amenable to therapeutic interventions. Further studies are required to define possible mediators of apoptosis (e.g., tumor necrosis factor or caspases) and therapies to inhibit them, as a method to reduce the cellular damage observed with ICH.

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