Is mannitol effective against platelet-activating factor (PAF)-induced liver damage in obstructive jaundice?

Platelet-activating factor, is a unique phospholipid with a broad range of biological activities that may be relevant in the development of inflammatory reactions. Platelet-activating factor has been suspected to play an important role in liver pathophysiology. The cultured Kupffer and endothelial cells produce and release platelet-activating factor in order to facilitate communication between hepatic sinusoidal and parenchymal cells. In this study, in the experimental jaundice model, platelet-activating factor levels were measured in liver tissue and plasma and the possible effects of mannitol on this mediator were assessed.

The experimental model consisted of 7 rats in the control group (CG), 7 rats in the sham operation group (ShG), and 7 rats in the obstructive jaundice group (JG) created by ligating the common bile duct. The last group was the mannitol-treated jaundiced group (MJG) and all animals in this group received 20% mannitol in doses of 2 mL/day, intraperitoneally, following common bile duct ligation. A week later all animals were sacrificed and plasma and liver tissue samples were collected. Platelet-activating factor levels were measured by radioimmunoassay technique.

Liver tissue platelet activating factor levels (pg/mg tissue protein) were 72 +/- 18 in the CG, 183 +/- 51 in the JG, 84 +/- 17 in ShG, and 124 +/- 36 in MJG. Plasma levels were 460 +/- 13, 1600 +/- 40, 560 +/- 19, and 1200 +/- 23, respectively. In both sample types, MJG and JG values were significantly different from CG and ShG as well. MJG levels were also different from JG.

These results showed that plasma and liver tissue platelet-activating factor levels are increased in experimental obstructive jaundice; and activation of this mediator contributes to the ongoing liver injury. Mannitol may improve or lessen this damage.