Shock (Augusta, Ga.) · 2026
Alteplase and Methylprednisolone Associated Treatment Modulate Microcirculation and Inflammation in Brain Death Donors.
СтатьяНазвание и аннотация: Перевод в очереди
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da Anunciação Lucas Ferreira, Vidal-Dos-Santos Marina, Fernandes Caio Medeiros, Ricardo-da-Silva Fernanda Yamamoto, de Assis Ramos Mayara Munhoz, Agostinho Brunella Valbão Flora, de Freitas Pedro Luiz Zonta, Breithaupt-Faloppa Ana Cristina, Correia Cristiano Jesus, Moreira Luiz Felipe Pinho
Аннотация
INTRODUCTION: Brain death (BD) triggers systemic inflammation, platelet aggregation, and thrombus formation, which compromise organ quality. This study evaluated the effects of the fibrinolytic alteplase alone and in combination with methylprednisolone, following BD induction.
METHODS: Wistar rats were randomized into four groups: sham (animals without BD), BD (animals subjected to BD), recombinant tissue plasminogen activator (rTPA) (animals with BD and alteplase treatment), and rTPA + P (animals with BD and alteplase and methylprednisolone treatment). The analyzed parameters included mesenteric microcirculation perfusion, inflammatory mediators, platelet aggregation, coagulation, and histology.
RESULTS: Improvements in mesenteric microcirculatory flow following alteplase were observed. This effect is likely related to the modulatory action of alteplase on platelet aggregation, along with an increase in vascular density, which occurred in association with a decrease in endothelin-1 levels. Combined therapy demonstrated an additional beneficial effect by modulating the inflammatory cascade, including significant reductions in Interleukin-6 (IL-6), Interleukin-10 (IL-10), and Vascular Endothelial Growth Factor, as well as improving leukocyte-endothelial interactions in the mesentery. Importantly, alteplase did not cause detectable damage to any of the studied organs.
CONCLUSION: Alteplase treatment prevented platelet aggregation and improved microcirculation. When combined with methylprednisolone, it also modulated the inflammatory response. These findings suggest that alteplase treatment has a potential benefit in maintaining the quality of brain-dead donors.
METHODS: Wistar rats were randomized into four groups: sham (animals without BD), BD (animals subjected to BD), recombinant tissue plasminogen activator (rTPA) (animals with BD and alteplase treatment), and rTPA + P (animals with BD and alteplase and methylprednisolone treatment). The analyzed parameters included mesenteric microcirculation perfusion, inflammatory mediators, platelet aggregation, coagulation, and histology.
RESULTS: Improvements in mesenteric microcirculatory flow following alteplase were observed. This effect is likely related to the modulatory action of alteplase on platelet aggregation, along with an increase in vascular density, which occurred in association with a decrease in endothelin-1 levels. Combined therapy demonstrated an additional beneficial effect by modulating the inflammatory cascade, including significant reductions in Interleukin-6 (IL-6), Interleukin-10 (IL-10), and Vascular Endothelial Growth Factor, as well as improving leukocyte-endothelial interactions in the mesentery. Importantly, alteplase did not cause detectable damage to any of the studied organs.
CONCLUSION: Alteplase treatment prevented platelet aggregation and improved microcirculation. When combined with methylprednisolone, it also modulated the inflammatory response. These findings suggest that alteplase treatment has a potential benefit in maintaining the quality of brain-dead donors.