Increasing attention has been given to the role of the lysosome in the pathogenesis of disease and tissue injury including shock. Lysosomes were described by de Duve1 in 1955 as biochemically inactive acid hydrolases, surrounded by an intact membrane. If the membrane becomes permeable or disrupted these enzymes are activated. Under certain conditions, concentrated lysosomal preparations can hydrolyse phosphate esters, ribonucleic acid (RNA), and microsomal and mitochondrial membrane components, causing loss of oxidative phosphorylation.2 For these reasons it has been suggested that lysosomes may play a major role in tissue destruction and may be the cause of irreversibility in shock.
Increase of lysosomal enzymes in the cytoplasm has been demonstrated biochemically in genetic muscular dystrophy,3 and shortly after ligation of the blood supply of a liver lobe.4 Slater and Greenbaum,5 however, were unable to detect rapid release of lysosomal enzymes after induction of acute liver necrosis.