Platelet Dynamics in the Sinusoid of the Liver after Ischemia-Reperfusion

Takafumi Tamura, Tadashi Kondo, Kiyoshi Fukunaga, Nobuhiro Ohkohchi


Hepatic ischemia-reperfusion (I/R) activates Kupffer cells (KCs), which produce various inflammatory cytokines, causing adhesion of neutrophils to sinusoidal endothelium and microcirculatory disturbance. These phenomena are well known as mechanisms of hepatic I/R injury. Recently, in the early period of I/R, i.e., within 120 min after reperfusion, it was proved that accumulation of platelets to sinusoid is strongly associated with mechanism of the I/R. In this editorial, we describe the mechanism of I/R injury focusing on platelets and KCs in the early period of I/R. We successfully observed the dynamics of platelets and KCs in the hepatic sinusoid time dependently using an intravital microscopy (IVM) system in rat. Platelets were isolated from the whole blood of syngeneic rats and labeled with rhodamine-6G. KCs were labeled using the liposome entrapment method. The observations revealed that platelets attached to KCs and sinusoidal endothelial cells (SECs) during the early period of I/R. The number of platelets adhering to both KCs and SECs increased in proportion to the duration of reperfusion. These interactions may be causally related to the downstream effects of I/R and are important to characterize. The existence of platelets as well as KCs is indispensable for the I/R injury.

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