[Is organ failure in hypovolemic-traumatic shock the result of the reperfusion syndrome or of other mediators?].

Decreased perfusion of vital organs is secondary to hypovolemic-traumatic shock and may lead to partial ischemia, which in turn causes nucleotide degradation and accumulation of hypoxanthine as well as the formation of xanthinoxidase. Thus, the pre-conditions for the development of detrimental oxygen radicals are set as soon as perfusion is reestablished. This could explain edema formation associated with the reperfusion syndrome, which is observed at least following total ischemia. Whether these reactions are responsible for edema formation secondary to shock, especially in endothelial cells, is being discussed with respect to the various organs. The present results indicate that damage to the organ occurs via lipid peroxidation due to the effect of oxygen radicals. The degree of involvement of the various sources of oxygen radicals--xanthinoxidase reaction, phagocytes--remains open. In all probability, the sources are involved to a different extent in the various organs. In the lung, the emphasis could be on the phagocytes (leucostasis, alveolar macrophages), in the muscle on the xanthinoxidase reaction. In addition, the numerous mediator systems should be taken into account, with particular emphasis on the unspecific proteolysis (especially through granulocyte elastase).