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

Background/Aims: Platelet-activating factor, is a unique phospholipid with a broad range of biological activities that may be relevant in the developm ent of inflammatory reactions. Platelet-activating factor has been suspecte d to play an important role in liver pathophysiology. The cultured Kupffer and endothelial cells produce and release platelet-activating factor in ord er to facilitate communication between hepatic sinusoidal and parenchymal c ells. In this study, in the experimental jaundice model, platelet-activatin g factor levels were measured in liver tissue and plasma and the possible e ffects of mannitol on this mediator were assessed. Methodology: The experimental model consisted of 7 rats in the control grou p (CG), 7 rats in the sham operation group (ShG), and 7 rats in the obstruc tive jaundice group (JG) created by ligating the common bile duct. The last group was the mannitol-treated jaundiced group (MJG) and all animals in th is group received 20% mannitol in doses of 2mL/day, intraperitoneally, foll owing common bile duct ligation. A week later all animals were sacrificed a nd plasma and liver tissue samples were collected. Platelet-activating fact or levels were measured by radioimmunoassay technique. Results: Liver tissue platelet activating factor levels (pg/mg tissue prote in) were 72 +/- 18 in the CG, 183 +/- 51 in the JG, 84 +/- 17 in ShG, and 1 24 +/- 36 in MJG. Plasma levels were 460 +/- 13, 1600 +/- 40, 560 +/- 19, a nd 1200 +/- 23, respectively. In both sample types, MJG and JG values were significantly different from CG and ShG as well. MJG levels were also diffe rent from JG. Conclusions: These results showed that plasma and liver tissue platelet-act ivating factor levels are increased in experimental obstructive jaundice; a nd activation of this mediator contributes to the ongoing liver injury. Man nitol may improve or lessen this damage.