Enzymohistochemical study on burn effect on rat intestinal NOS.

Abstract

The blood irrigate flow obstruction, especially the gastrointestinal (GI) ischemia[1], is the main factor of the damage to the digestive tract caused by serious burns. The effect of GI ischemia on the whole body is extensive and profound, which not only causes the increase of intestinal permeability and the movement of bacteria and toxin in the intestinal cavity, but releases a large quantity of inflammatory media. Neuroendocrine element after burns is closely related to intestinal damage[2]. As is known at present, abundant nitric oxide synthase (NOS) is distributed in GI tract, whose product NO is a nonadrenergic and noncholinergic (NANC) restraining transmitter in enteric nervous system which participates extensively in various physiological functions in the intestinal tract[3]. Few reports about the effects on intestinal NOS after serious burns are available. We used scalded rat model with degree III 40% of body surface area (TBSA), and enzymatic histological and biochemical methods to observe dynamically the active changes of empty myenteric plexus NOS and changes of jejunal tissue MDA SOD and GSH-PX and probe into the relationship between NOS and intestinal tissue and function damage as well as their mechanism so as to provide morphological experimental basis for clinical treatment.