[Study on preserving intestinal function and the possible mechanism of hypermetabolic response following severe burn injury].

In order to approach the mechanism of hypermetabolic response following severe burn injury, a new animal model was developed with a specially bred miniswine (Guizhou species). Multiple catheterizations were applied for sampling different blood from portal, inferior mesenteric as will as jugular (central) veins. The animals were sustained with 30% III burn of TB-SA and divided randomly into early feeding group, given a complete diet beginning from 2 hours postburn (N = 6), and delayed feeding group, given the same diet initiating on 4 day postburn (N = 6). The results showed that compared with delayed feeding, early enteral feeding could strengthen the barrier function, decline the rate of translocation of bacteria and endotoxin from the gut to portal vein, reduce obviously blood TNF, CRP and catabolic-hormones, and significantly decrease REE (resting energy expenditure) and urinary 3-Mehis excretion. During the hypermetabolism (PBD7-10), the metabolic response mediated by "intestinal way" was at least 35%. The way of "intestinal tract--macrophages in liver--Hypermetabolism" is a possible mechanism of hypermetabolic response following severe burn injury, and the bacteria and endotoxin translocated from the gut, the active products (IL-1, TNF, etc) released by Kupffer's cells might be the mediating factors of the mechanism.