The concepts of 'burn toxaemia' and 'auto-intoxication' are defined within the relationship between burns and the 'toxaemic phase'. This 'intoxication' can be the result of the presence and action of a purely 'toxic' substance, but also of any other substance of different nature and varying mechanism, already present in the organism as a precursor or newly formed at the site of the burn or at a distance. Rather than an attempt to isolate a single toxic substance after burns, this research involved a study of the most important and elementary mechanisms of the detoxicating metabolism of the liver for endogenous and exogenous chemical compounds; the oxidative microsomial system. Wistar rats were burned by a standard technique. liver was then removed at intervals. Cytochrome P-450 and its fractions (fundamental elements of the oxidative microsomial system) were measured. At the same time morphological controls were carried out with the optic and electron microscopes. Six hours after the burn the total concentration of cytochrome P-450 increased by 20%. The dithionite-reducible component dropped by 40% while the TPNH-reducible increased by 80%. Histologically, hepatic damage was noted with widespread changes in the endoplasmic reticulum and mitochondria. This indicated the increased need for microsomial oxidation and induction of the cytochrome P-450 by a 'toxic substance'. At the 24th hour both histological and functional liver damage were less evident, indicating a halt of induction stimulus on the oxidative system of the hepatic microsomes, probably due to inactivation of the 'toxic factor' by cytochrome P-450. These data confirm, indirectly, the hypothesis, proposed by different workers, that the 'toxic factor', glycoprotein, lipoprotein or some other substance reacts early on in the pathogenesis of the burned state causing parenchymal damage of the liver in the immediate period after the burn.
|Number of pages||21|
|Journal||Rivista Italiana di Chirurgia Plastica|
|Publication status||Published - 1979|
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