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  • Title: Small intestinal motility disorders in preruminant calves chronically fed a diet based on antigenic soya: characterization and possible mediators.
    Author: Lallès JP, Duvaux-Ponter C, Sissons JW, Toullec R.
    Journal: Vet Res; 1998; 29(1):59-72. PubMed ID: 9559521.
    Abstract:
    Intestinal motility disorders and some mediators implicated in these disorders were studied in preruminant calves that had been chronically fed a diet containing an antigenic heated soyabean flour (HSF) for 3 months. The calves in the present study had previously been shown to present strong immune reactions against soyabean proteins, as assessed through plasma antibody titres, direct skin tests and in vitro lymphoproliferation. Four of these calves sensitive to soya were fitted with an abomasal catheter and wire electrodes on the jejunum. Myoelectric activity was recorded over 7 h following test meals containing skim milk powder (SMP), HSF or a non-antigenic hydrolysed soya protein isolate (HSPI). The pattern of myoelectric complexes migrating to the jejunum was regular with SMP (mean durations of phases I, II and III: 26, 38 and 5.28 min, respectively). With HSF, diarrhoea appeared, and the total duration of phase I decreased from 149 to 68 min (P < 0.01) while that of phase II increased from 239 to 328 min (P < 0.01). The mean duration of phase III decreased from 5.3 to 3.9 min (P < 0.01). These changes, including diarrhoea, were substantially reversed by feeding HSPI. When promethazine, a H-1 histamine receptor antagonist, was administered i.v. prior to feeding HSF the number of phases I tended to decrease and diarrhoea virtually disappeared. In contrast, indomethacin, a cyclooxygenase inhibitor, had limited effects on motility patterns and diarrhoea. These disorders were partially reproduced by i.p. administration of platelet-activating factor (PAF) prior to feeding with SMP. These findings suggest that calves chronically fed antigenic soya suffer from immune-mediated motility disorders which are linked to histamine action via H-1 receptors, and possibly with PAF. The role of arachidonic acid catabolites of the cyclooxygenase pathway is probably minor.
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