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

Hepatic ischemia-reperfusion (I/R) activates Kupffer cells (KCs),which produce various inflammatory cytokines, causing adhesionof neutrophils to sinusoidal endothelium and microcirculatorydisturbance. These phenomena are well known as mechanisms ofhepatic I/R injury. Recently, in the early period of I/R, i.e., within120 min after reperfusion, it was proved that accumulation of plateletsto sinusoid is strongly associated with mechanism of the I/R.In this editorial, we describe the mechanism of I/R injury focusingon platelets and KCs in the early period of I/R. We successfullyobserved the dynamics of platelets and KCs in the hepatic sinusoidtime dependently using an intravital microscopy (IVM) system inrat. Platelets were isolated from the whole blood of syngeneic ratsand labeled with rhodamine-6G. KCs were labeled using the liposomeentrapment method. The observations revealed that plateletsattached to KCs and sinusoidal endothelial cells (SECs) duringthe early period of I/R. The number of platelets adhering to bothKCs and SECs increased in proportion to the duration of reperfusion.These interactions may be causally related to the downstreameffects of I/R and are important to characterize. The existence ofplatelets as well as KCs is indispensable for the I/R injury.