Recently, organ-specific Shwartzman reaction was appeared in the literatures. Shwartzman reaction have thought to be ischemic injury by fibrin thrombi formation in small vessels. But in some part the participation of cellular elements, such as
Kupffer
cells and infiltrated neutrophilc and mononuclear phagocytic cells. This study was carried out to induce a selective liver necrosis by Shwartzman mechanism and to investigate the rele of prostaglandin E2 known to be a cytoprotector, on the
endotoxin
liver injury.
Challenge doses of 0.2mg of endotoxin emulsified in Lipiodol were given to right lateral lobe of rabbits via portal vein and provocation doses of 0.02mg/kg via ear vein 24 hours later(Group 1). Some of the animals received additionally
heparin(Group 2),
PGE2(Group 3) and indomethacin injection(Group 4), respectively, Control group(Group 5) received only saline for provocation. Livers were extracted out 24 hours after last injections and examined by gross, light and electron microscopes.
@ES The results were summarized as follow:
@EN Four animals were died during operation: two animals after challenge injection; five animals in Group 1; and one animals in Group 4.
Grossly selective liver necroses were found on the right lateral lobe sparing other lobes in all animal groups. The extent of necroses were most severs in Group 1 animals: Next in order of Group 4, Group 3, Group 2 and Group 5.
Light microscopic examination revealed two types of necrosis, pure coagulation necrosis without inflammatory changes and those associated with massive inflammatory infilration and liquefaction necrosis. Both type of necroses was found in Group 1
animals, while inflammatory type predominated in Group 2 and coagulation type in Group 3. Group 4 animals showed approximately equal degree of changes of both type of necrosis, but milder than Group 1.
Electon microscpic examination showed occlusions of sinusoid by fibrin thrombi, necrotic cellular debris, inflammatory infiltrates and hypertrophied Kupffer cells. Kupffer cells were enlarged and activated with formation of cytoplasmic processes.
Drop
out necrosis were noted in the liver cells near the inflammatory infiltrates.
The results suggested that endotoxin provokes two mechanisms of liver cells necrosis: ischemic and cellular. Heparin may reduce ischemic injury and PGE2 may decrease injury exerted from inflammatory cells.
Shwatzman Reaction Key wards: Liver, Endotoxin Prostoglandin.
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