An interpretation of many of the classical signs of ruminal dysfunction is possible by extrapolation from the results of research in rumen physiology. Correlation of motility and ruminal fluid characteristics will often provide a means of establishing the degree, the duration and the differential diagnosis of the dysfunction detected. In the case of disorders of ruminal motility, general anaesthesia and diseases at any sites which produce pain or fever can inhibit the hindbrain reflex centres responsible for evoking primary and secondary cycle contractions of the reticulorumen. Simple indigestion/rumen impaction, vagus indigestion and hypocalcaemic milk fever cause ruminal stasis, probably because they relax the reticuloruminal smooth muscle and hence decrease the reflexly excitable sensory inputs from tension receptors. Grain engorgement/ruminal acidosis and extreme bloat are likely to excite other sensory receptors (epithelial receptors), which reflexly inhibit cyclical motility. Bloat occurs when eructation is inadequate either because the oesophagus is obstructed or because cardiac opening is reflexly inhibited by the presence of ruminal fluid rather than gas at the cardia in conditions of subnormal motility or of leguminous frothing.
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