흰쥐에서 急性出血性 쇽에 의한 血小板 形態 變化의 電子顯微鏡的 觀察 = Transmission Electron Microscopic Observation in Rat Platelet Responded to Hemorrhagic Shock

다국어 초록 (Multilingual Abstract)

Experimental studies have suggested that increased and liberated lysosomal enzymes contribute directly to the pathophysiology of hemorrhagic shork by exerting a splanchnic vasoconstrictor effect in the pancreas and in the entire splanchnic region.
The major sources of these enzymes are thought to be the intestinal epithelium, liver, pancreas, spleen or kidney.
On the other hand, blood platelet also contain large amount of lysosomal enzymes.
Response of rat platelet to hemorrhagic shock was examined through using ultrastructural technique.
The blood platelet of the rat pretreated with saline responded to hemorrhagic shock with decrease of α-granules and the development of the platelet canalicular system which opens to the extracellular environment and the pseudoped formation .
So, these facts suggest that the granules observed to be released from platelet have strongly contributed to the rise in serum lysosomal enzyme.
Glucocorticoid has been considered controversial in the treatment of hemorrhagic shock.
Glucocorticoid, however, seems to stablized lysosomal membranes, providing cellular protection in hemorrhagic shock.
The effect of dexamethasone almost completely inhibited morphological alterations in rat platelet 180 minutes after induction of hemorrhagic shock, and delayed the decrease of α-granules.