Effects of scald injury on hepatic PO2, blood flow, and ultrastructure in the rat.

Stagnant hypoxia has been suggested as a significant factor underlying acute liver disease following thermal injury. To examine this possibility in circumstances of moderate scald injury, rats were dipped (15% body surface area) in 90-95 degrees C water for 25 sec, fluid resuscitated, and studied at 1, 6, and 24 h. Hepatic PO2, obtained by multicathode surface measurement, was reduced significantly at 1 h (10.8 vs. 20.8 mm Hg in controls), although clearance times for low dose indocyanine green (ICG) suggested normal liver blood flow. The reduction of PO2 was transient; at 6 h levels were only slightly lower than in controls. At 24 h, however, liver PO2 was again reduced significantly, albeit less deeply (14.9 mm Hg). Increased clearance times for low and high dose ICG at 24 h suggested impairment of both blood flow and hepatocyte function. Hepatic ultrastructure showed foci of cells with anomalous and degenerate mitochondria, atypical of those associated with hypoxia. Sinusoids were often occluded by aggregates of vesicles of hepatocyte origin. It is not clear that acute restriction of oxygen availability during the first hour postburn was of sufficient intensity to cause the liver pathology evident at 24 h.