Role of microcirculation in hepatic ischemia/reperfusion injury.
There is a large body of evidence that the liver microcirculation has to be considered as a major target in hepatic ischemia/reperfusion injury. The nature of microvascular injury, which precedes manifestation of hepatic parenchymal tissue damage, includes both hypoxia due to lack of microvascular perfusion (i.e. no-reflow), and a reperfusion-associated inflammatory response, which includes the activation and dysfunction of leukocytes and Kupffer cells (the reflow paradox). No-reflow in sinusoids is thought to be caused by endothelial cell swelling and intravascular hemoconcentration, and involves also a deterioration of the balance between ET and NO. The reflow paradox is associated with: (i) the release and action of proinflammatory cytokines (TNF-alpha, IL-1) and oxygen radicals; (ii) the up-regulation of endothelial and leukocytic adhesion molecules (selectins, beta-integrins, ICAM-1); and (iii) the interaction of leukocytes with the endothelial lining of the hepatic microvasculature.
Menger
M D
MD
Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany.
Richter
S
S
Yamauchi
J
J
Vollmar
B
B
D000818:Animals; D019332:Endothelin-1 / Q000502:physiology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D007375:Interleukin-1 / Q000502:physiology; D007728:Kupffer Cells / Q000502:physiology; D007962:Leukocytes / Q000502:physiology; D008099:Liver / Q000098:blood supply*; D008833:Microcirculation / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D017382:Reactive Oxygen Species / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology*; D019087:Selectins / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D019332:Endothelin-1; D007375:Interleukin-1; D017382:Reactive Oxygen Species; D019087:Selectins; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide