Abstract
Lysosomes are subcellular organelles containing various acid hydrolases and isolated from the surrounding cytoplasm by a single lipoprotein membranes. Hypoxia and acidosis are main factors known to increase the fragility of the lysosomal membrane. Splanchnic ischemia during circulatory shock provides the ideal circumstances for the activation and extra-lysosomal release of these enzymes.
Intracellular redistribution of hydrolases causes mitochondrial dysfunction in the reversible stage and cellular death in the terminal stage. Enzymes released extracellularly induce injury to tissues distant from their site of origin, and produce MDF and other vasoactive polypeptides through proteolysis. Leucocytes trapped in the pulmonary capillary beds in shock cause capillary damage and increase the permeability by the disruption of lysosomes.
Clinical and laboratory studies have demonstrated a salutary effect of steroids on shock state through the stabilization of lysosomal membrane. Aprotinin known as effective inhibitor of acid proteases is effective for the prevention and reversal of shock.
These results show that lysosomal acid hydrolases play an important role in the pathogenesis of refractory shock.
