Portal Infusion of Low Dosage Endotoxin: A Model Simulating Translocation of Ruminai Endotoxin in Cattle

Abstract

Translocation of bacteria and endotoxin from the gastro-intestinal tract to the portal blood is described to occur in healthy humans and animals, and is probably facilitated by ruminai epithelium damage in cattle (Berg 1992). Controversy exists regarding the possible role of endotoxin in the pathogenesis of ruminai acidosis. Systemic disease during ruminai acidosis is clinically characterized by forestomach stasis, anorexia, depression, tachycardia, tachypnea and fever. It has been shown that blood concentrations of arachidonic acid metabolites increase during ruminai acidosis, which may explain many of these clinical signs (Andersen et al. 1994). At the same time, we found that only few cows with experimentally induced rumen acidosis had endotoxin in the systemic blood (Andersen et al. 1990, 1994), while other authors describe systemic endo-toxaemia as an occasional finding in similar or milder cases of grain-engorgement (Boosman et al. 1990, Aiumlamai et al. 1992). Arachidonic acid metabolites are readily produced in the presence of endotoxin, but might also be expected to be produced during a chemical inflammation process of ruminai epithelium, damaged by a low pH and high osmolar concentration. The purpose of the present study was to evaluate the role of low grade portal endotoxaemia for pre-hepatic release of inflammatory mediators 6-ketoprostaglandin F_1a (6-keto-PGF) and thromboxane B₂ (TXB) and the relation to systemic disease. Four healthy cows were surgically equipped with chronic catheters in the portal vein, in a mesenteric vein 20 cm distally to portae hepa-tis and in a hepatic vein. After recovery, the cows received at maximum 3 different treatments at monthly intervals in a randomized design. Treatments were saline solution infused into the mesenteric vein at 2.5 üL/kg body weight per min (control), Escherichia coli endotoxin (055:B5 Westphals extraction, Sigma) at 0.025, 0.25 and 2.5 ng/kg body weight per min (Model I, Model II and Model III, respectively, Table 1). Infusions were continued for 180 min, or until respiratory distress (respiration rate > 40 per min) occurred. One h before a session, a jugular catheter was inserted, and blood samples were collected from the portal, hepatic and jugular vein for determination of clinical-chemical parameters (acid-base balance, packed cell volume (PCV), leukocyte and thrombocyte counts), endotoxin, TXB and 6-keto-PGF. Methods are described elsewhere (Andersen et al. 1994). After initiation of the experimental infusion, sampling was continued for 330 min at intervals of 30 min. Clinical parameters (rectal temperature, pulse and respiratory rates and ruminai movements) were determined hourly.