Microvascular research · 2026
Fucoidan preserves endothelial glycocalyx and reduces microvascular obstruction after myocardial ischemia-reperfusion.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Fernandes Pedro Lucas Moreira, de Castro Silva Patrícia Alves, Miranda Carlos Henrique
Аннотация
INTRODUCTION: Ischemia-reperfusion (I/R) injury induces microvascular obstruction (MVO). The endothelial glycocalyx (eGC) is crucial for maintaining microvascular homeostasis. Fucoidan (FCD), a heparan sulfate mimetic, may protect the eGC. This study investigated whether FCD preserves the eGC and attenuates MVO following myocardial I/R.
METHODS: Isolated rat hearts were perfused using a Langendorff apparatus and allocated to four groups: Sham (S), perfused with Krebs-Henseleit (KH) solution for 80 min; Sham + FCD (S + F), with FCD added during the final 40 min; I/R, consisting of 10 min perfusion, 30 min global no-flow ischemia, and 40 min reperfusion; and I/R + FCD (I/R + F), treated as I/R with FCD administered throughout reperfusion.
RESULTS: FCD administration during reperfusion significantly reduced MVO compared with I/R alone. Transmission electron microscopy revealed preservation of the eGC in the I/R + F group. Pericapillary edema was significantly decreased with FCD treatment. Additionally, nitrite levels were significantly higher in the I/R + F group during both early and late reperfusion.
CONCLUSION: FCD attenuates MVO after myocardial I/R injury by preserving the eGC, reducing pericapillary edema, and restoring nitric oxide bioavailability.
METHODS: Isolated rat hearts were perfused using a Langendorff apparatus and allocated to four groups: Sham (S), perfused with Krebs-Henseleit (KH) solution for 80 min; Sham + FCD (S + F), with FCD added during the final 40 min; I/R, consisting of 10 min perfusion, 30 min global no-flow ischemia, and 40 min reperfusion; and I/R + FCD (I/R + F), treated as I/R with FCD administered throughout reperfusion.
RESULTS: FCD administration during reperfusion significantly reduced MVO compared with I/R alone. Transmission electron microscopy revealed preservation of the eGC in the I/R + F group. Pericapillary edema was significantly decreased with FCD treatment. Additionally, nitrite levels were significantly higher in the I/R + F group during both early and late reperfusion.
CONCLUSION: FCD attenuates MVO after myocardial I/R injury by preserving the eGC, reducing pericapillary edema, and restoring nitric oxide bioavailability.