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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.
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Systemically, excessive NO levels lead to hypotension [12],[13], microcirculatory dysfunction [14], and refractoriness to vasopressor catecholamines [15].
SAKI, however, is determined by a complex and highly treatment-dependent interplay between inflammation, microcirculatory dysfunction, bioenergetic failure, and tubular cell adaptation to injury [3].
Acute inflammatory injury incites a cascade of proinflammatory mediators leading to microcirculatory dysfunction, capillary leak, and distributive shock [1, 2].
Acute inflammatory injury incites a cascade of proinflammatory mediators leading to microcirculatory dysfunction, capillary leak, and distributive shock [ 1, 2].
Endothelial injury has emerged as a crucial early event in the pathogenesis of microcirculatory dysfunction, capillary leakage and multiorgan dysfunction syndrome.
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