Role of microcirculation in hepatic ischemia/reperfusion injury.

摘要: Abstract There is a large body of evidence that the liver microcirculation has to be considered as major target in hepatic ischemia/reperfusion injury. The nature microvascular injury, which precedes manifestation parenchymal tissue damage, includes both hypoxia due lack perfusion (i.e. no-reflow), and reperfusion-associated inflammatory response, activation dysfunction leukocytes Kupffer cells (the reflow paradox). No-reflow sinusoids thought caused by endothelial cell swelling intravascular hemoconcentration, involves also deterioration balance between ET NO. paradox associated with: (i) release action proinflammatory cytokines (TNF-alpha, IL-1) oxygen radicals; (ii) up-regulation leukocytic adhesion molecules (selectins, beta-integrins, ICAM-1); (iii) interaction with lining microvasculature.