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Appropriate enteral nutrition provided immediately after injury or trauma to the gastrointestinal tract may limit or reverse damage to the mucosal barrier. In this regard, diets containing amino acids, such as arginine and glutamine, or fish oil have been identified as beneficial. This report assesses the role of amino acids as "essential nutrients" in the repair of intestinal mucosa damaged by gamma radiation. Rats were used experimentally to test the hypothesis that the recovery of the immune responses in the intestinal mucosa, which are suppressed by radiation, can be improved by feeding an elemental amino acid diet, referred to hereafter as the diet, immediately after irradiation. The objective was to assess the impact of the diet on the expression of type I hypersensitivity or anaphylaxis in the jejunal mucosa. The local expression of this immunological response, which involves several radiosensitive cell types, was studied in rats immunized by oral infection with the nematode parasite, Trichinella spiralis. Rats that recover from infection become immunized and their small intestine undergoes anaphylaxis when subsequently challenged with parasite-derived antigen. This hypersensitivity response is expressed, in part, as Cl- secretion and can be observed in vitro or in vivo. When challenge is provided by a secondary inoculum of infective T. spiralis larvae, Cl- secretion is accompanied by fluid secretion and by the rapid expulsion of the parasite from the intestine. Immunized rats maintained on a stock diet and exposed to 7 Gy of total-abdominal irradiation from a cobalt-60 gamma-ray source failed to express antigen-induced Cl- secretion fully for up to 14 days postirradiation, and rejection of the parasite was suppressed for at least 30 days postirradiation. The suppression of immune responsiveness is associated with the disappearance of intestinal mucosal mast cells, which normally trigger the anaphylactic response. When rats are maintained on the diet after irradiation, the capacity to reject the parasite remains suppressed. However, the ability to express anaphylaxis-mediated Cl- secretion returns by 3 days postirradiation. The quick, diet-supported recovery of antigen-induced Cl- secretion occurs despite the continued absence of mast cells. Although the recovery of anaphylaxis-mediated responses suppressed by irradiation is only partial, our experimental results underscore the potential for enhancing the recovery process through nutritional support.
Anaphylaxis-mediated intestinal fluid secretion was measured in Trichinella spiralis- or ovalbumin-immunized rats challenged intraduodenally with T. spiralis somatic antigen (1 mg protein/0.5 mL saline) or ovalbumin (1 mg/0.5 mL saline), respectively. Intestinal fluid volume was measured 30 minutes after challenge as an index of net secretion. Challenge with the antigenic bolus containing 40 mmol/L D-glucose induced twice the fluid secretion as that induced by either antigen alone. L-Glucose was an ineffective substitute for D-glucose. The enhancement of secretion by D-glucose was dependent on prior immunologic sensitization, was diminished in the presence of phlorizin, and was mimicked by beta-methyl glucoside. Results indicate that the active transport of D-glucose augments the antigen-mediated fluid secretion, possibly by enhancing permeation of the intestinal epithelium to antigen, thereby providing greater access to the mucosal immune system.
Experiments were performed on chloralose anaesthetized cats. Biliary and pancreatic secretions were diverted by separate cannulation of each duct. A 2-cm segment of the proximal duodenum was isolated between two luminally situated balloons and perfused with isotonic saline containing 14C-PEG 4000 as a non-absorbable marker. The perfusate was analysed with regard to alkalinity (back titration) and concentration of marker (liquid scintillation). Net alkalinization and net fluid transport were calculated with conventional equations. Motor activity in the duodenal wall was recorded as changes in volume of the proximal balloon. Exposing the duodenal segment of 30 mM HCl induced duodenal contractions, net fluid secretion and an increased alkaline secretion, responses which were insensitive to acute truncal vagotomy. The acid-induced increase in contraction frequency was inhibited by hexamethonium, but not by atropine. Alkaline secretion in response to luminal acid was blocked by hexamethonium and inhibited by atropine, whereas the net fluid secretion was insensitive to these compounds. It is concluded that luminal exposure to hydrochloric acid changes the duodenal functional state by mechanisms which are independent of the extrinsic neural supply. Duodenal contractions during luminal acid exposure, and the alkalinization after such acid exposure, are mediated via local neural pathways, involving a nicotinic cholinergic step and, to some degree, muscarinic transmission. The mucosal volume secretion, however, appears to be mediated by non-conventional mechanisms.
The ascites fluid secreted by the isolated perfused liver was studied in rats. The quantity of fluid appearing on the surface of the isolated perfused liver was independent of the pressure in the portal vein and could be raised by the amount of fluid flowing through the liver. Irrespective of the flow conditions, the ischaemic liver will produce more ascites than the intact liver und similar conditions. A rise of hepatic oncotic pressure will not reduce ascites production by the ischaemic liver. With respect to osmolarity there is no difference between the perfusing fluid and ascites. As regards the quantity of bilirubin secreted with ascites no significant difference was found between the control and the ischaemic group. The pertaining literature and the theories of ascites formation are discussed.