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Endothelial activation alters vascular tone and induces both microcirculatory dysfunction and coagulopathy, which will in turn favor ischemic and/or hemorrhagic lesions [34].
Endothelial activation alters vascular tone and induces both microcirculatory dysfunction and coagulopathy, which will in turn favor ischemic and/or hemorrhagic lesions [ 34].
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Excessive release of pro-inflammatory mediators and disturbances in the coagulation system are believed to be involved in the pathogenesis of sepsis; both leading to microcirculatory dysfunction and consequent organ failure [6, 7].
Microcirculatory dysfunction and coagulopathy are both consequences of endothelial activation [ 1, 24] but are not easily preventable or treatable.
In addition, reperfusion brings microcirculatory dysfunction and disturbed oxygen handling [21, 22].
Arterial underfilling, microcirculatory dysfunction, and secondary interstitial edema lead to systemic hypoperfusion and impaired regional tissue oxygenation [2].
Microcirculatory dysfunction and organ perfusion were assessed through arterial lactate level, urinary output, mottling score and knee capillary refill time.
Without anemia or hypoxia, low PbtO2 despite adequate CBF probably reflects microcirculatory dysfunction and pericapillary edema [17].
Brain death in organ donors alters central hemodynamic performance, impairs physiology, exaggerates inflammation, and causes end-organ microcirculatory dysfunction and hypoxia.
Brain dead organ donors have altered central hemodynamic performance, impaired hormone physiology, exaggerated systemic inflammatory response, end-organ microcirculatory dysfunction, and tissue hypoxia.
in addition, there are data showing that microcirculatory dysfunction and Cellular metabolic alterations are associated with mortality and can fuel tissue distress leading to organ dysfunction [1].
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