Liver ischemia/reperfusion induces an increase of microvascular leukocyte flux, but not heterogeneity of leukocyte trafficking

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Abstract
Leukocytic response plays a major role in the manifestation of hepatic ischemia/reperfusion (I/R) injury. To clarify whether post‐ischemic hepatic leukocyte accumulation is based on increased leukocyte flux to the hepatic tissue due to systemic inflammation or chemoattractant activities or whether it represents solely a local tissue response without changing overall leukocyte flux and trafficking characteristics through the microvasculature, we studied acinar and sinusoidal leukocyte flux and distribution in rat livers in vivo both under normal (sham, n=8) and post‐ischemic (60′ ischemia/75′ reperfusion) conditions (I/R, n=8), using fluorescence epi‐illumination microscopy (rhodamine‐6G). Hepatic ischemia/reperfusion significantly (ppp<0.01) fraction of polymorphonuclear leukocytes (65.2±11.2%) and stab cells (9.5±7.9%) during post‐ischemic reperfusion when compared with sham controls (8.8±3.5% and 0.2±0.4%) was demonstrated. Thus, the increase of hepatic leukocyte flux after ischemia/reperfusion may be the result of both the manifestation of a systemic inflammatory response and the increase of local chemoattractant activities, such as the production and release of the cytokine‐induced neutrophil chemoattractant of the IL‐8 family.

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