Ruminal Stasis Research Articles

A possible role of endotoxins in spontaneous paretic cows around parturition.

Six late pregnant old cows which had a history of parturient paresis were studied with respect to clinical and blood biochemical changes during two weeks before and after parturition. The levels of serum endotoxin were evaluated during two days before and after parturition. Three out of six animals showed signs of paresis and two animals needed treatment. The clinical and general changes of all parameters supported the idea that during parturient paresis and parturition, there is absorption of endotoxins from the gastro-intestinal tract. Most of the studied parameters changed similarly to what has been described in experimentally induced endotoxaemia. The animals showed signs of ruminal stasis, had an increase in body temperature, prostaglandin metabolite and endotoxin as well as a decrease in serum calcium, zinc, iron and bile acids levels. The changes of these parameters were also closely related to each other. Furthermore, the changes were more pronounced in paretic cows. Endotoxins absorbed from the gastro-intestinal tract can be involved in paresis and make the outcome of this disease more severe.

The Influence of Flunixin on the Response to Salmonella typhimurium Endotoxin in Calves

The effects of intravenous injection of 0.5 microgram/kg body weight of Salmonella typhimurium endotoxin were studied in calves. The injection was followed by ruminal stasis and general dullness. The clinical signs disappeared within 24 hours. The injection was followed by a tremendous increase in the plasma level of 15-ketodihydro-PGF2 alpha, the main metabolite of PGF2 alpha. The injection was also associated with a profound leukopenia and significant decreases in the serum levels of iron, zinc and calcium. In order to study the role of prostaglandin (PG) for the development of endotoxin-induced changes a group of calves was pretreated with flunixin, a potent cyclo-oxygenase inhibitor, at a dose of 2.2 mg/kg body weight. Flunixin inhibited the PG release completely, but did not influence the other responses to endotoxin. The pyrogenic response to endotoxin was very moderate and it was suggested that fever is not the most suitable parameter for monitoring endotoxin effects in calves. The studied blood parameters (15-ketodihydro-PGF2 alpha, iron, zinc, calcium and the number of leukocytes) appeared to be much more sensitive.

Loss of Forestomach Motility in Sheep Experiencing Ruminal Lactic Acidosis is not Dependent on Duodenal Acidification by Lactic Acid

Reticuloruminal motility, duodenal myoelectrical activity, and the pH and lactic acid concentrations of ruminal and duodenal contents were monitored in rumen fistulated sheep that were intraruminally loaded with finely ground wheat (50 g/kg). Following ruminal loading, reticuloruminal motility was enhanced. However, within 6 hours of loading, forestomach motility was impaired and within 9 hours ruminal stasis occurred. During loss of forestomach motility, lactic acid concentrations in ruminal contents increased and may, in part, have contributed to the decrease in pH of ruminal fluids. The levels of lactic acid within duodenal contents also rose, however, the pH of duodenal contents remained unchanged. During the loss of reticuloruminal motility, premature regular spiking activity (RSA) and/or abnormal patterns of migrating myoelectric complexes (MMC) were not observed on the duodenum. These findings indicate that loss of forestomach motility in ruminal lactic acidosis may not be a consequence of acidification of the proximal duodenum by lactic acid produced in the forestomach.

Current ideas on the pathophysiology and treatment of lantana poisoning of ruminants.

Lantana poisoning in ruminants results from the ingestion of toxic varieties of the plant Lantana camara, which contain the triterpene acids lantadene A and lantadene B. Poisoning results in intrahepatic cholestasis and the consequences of the liver injury include jaundice, photosensitisation and ruminal stasis. The decreased ruminal motility causes toxic material to be retained in the rumen and continuous absorption of toxins from the rumen maintains the disease. Lantana poisoning can best be treated by preventing further absorption of toxins. This can be achieved by giving a large quantity of activated charcoal into the rumen together with a large volume of a multiple electrolyte solution to stimulate ruminal motility and rehydrate the animal. Treatment for photosensitive dermatitis should also be given.

FORESTOMACH EPITHELIAL RECEPTOR ACTIVATION BY GRAIN OVERLOAD RUMEN FLUIDS

Rumen fluids, obtained during the loss of forestomach motility in sheep experiencing ruminal lactic-acidosis, activated reticulo-ruminal epithelial receptors when applied to the receptive fields of these receptors. Rumen fluids which contained the highest levels of undissociated volatile fatty acids (VFAs) were the most effective. Since the levels of undissociated VFAs in effective rumen fluids were, in some cases, lower than the determined VFA thresholds of the receptors, receptor activation in these instances may have been facilitated by the levels of free lactic acid within these samples. Key words: Grain overload, epithelial receptors, ruminal stasis

The mechanism of ruminal stasis in lantana-poisoned sheep.

The effect of poisoning by the plant Lantana camara L. on reticulo-ruminal motility was investigated in sheep. There was a marked decrease in forestomach motility 4-6 h after dosing with the plant and motility continued to be depressed throughout the course of the disease. The effect of lantana on motility was characterized by a decrease in the number and median amplitude of forestomach movements. This was in contrast to the effect of starvation which caused a decrease in only the number of forestomach movements and even this effect was less severe than in lantana-poisoned animals. The effects of lantana on the components of the reflex which controls rumen motility were examined. No evidence was found for a direct effect of lantana toxins on the stretch and tactile receptors in the reticulum; on the vagus nerves; on the gastric centre or on the muscle of the forestomach. However, evidence was found to support an hypothesis that stasis of the rumen in lantana poisoning is due to inhibitory influences arising from the damaged liver. The evidence included a correlation between the onset of ruminal stasis and liver injury; a relationship between the severity of liver injury and ruminal stasis and the finding that denervation of the liver converted the pattern of forestomach movements in intoxicated animals to that seen in starved animals. It is concluded that stasis of the rumen in lantana-poisoned animals is due at least initially, to inhibitory neural impulses arising from the damaged liver and to the effects of anorexia.

Clinical diseases of the rumen: a physiologist's view.

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.

Current aspects of the primary insufficiency of the motor functions of the reticulum and rumen

Until the middle of this century the diagnosis “hypotony” or “atony” of the rumen was one of the most frequent diagnoses in veterinary practice. Rumen atony was considered as a primary disease and its removal was considered as the definitive therapeutic task. Subsequently it has been demonstrated that a great number of digestive disorders as well as other organic or general diseases can inhibit reticulo-ruminal motility. On the basis of our present knowledge the following disorders of the rumen and reticulum can be coordinated to the definition (term) Indigestion. At first primary and secondary indigestions have to be distinguished. The primary indigestions can be subgrouped into motor dysfunctions and disorders of the microbial-biochemical digestion. The primary disorders of the motor functions of the rumen and reticulum can be differentiated presently. Today the question arises whether a primary, a genuine ruminal stasis, really exists or at least whether conditions exist in which the inhibition of the motility of the forestomachs can be considered as the definitive finding.

Role of circulating prostaglandins in the genesis of pyrogen (endotoxin)‐induced ruminal stasis in conscious goats

Role of circulating prostaglandins in the genesis of pyrogen (endotoxin)‐induced ruminal stasis in conscious goats

The effect of flurbiprofen upon fever and ruminal stasis induced by Escherichia coli endotoxin, Poly I: Poly C and sodium nucleinate from yeast in conscious goats

Intravenous injection of endotoxin from Escherichia coli (0.01 μg and 0.1 μg per kg body weight), sodium nucleinate from yeast (5 mg and 10 mg per kg body weight) or Poly I: Poly C (15 μg and 30 μg per kg body weight) caused fever, changes in heart rate and stasis of the extrinsic ruminal contractions in conscious goats. It appears that ruminal stasis is associated with clinical and experimental fever. The febrile responses were abolished by the prior intravenous administration of flurbiprofen (2 mg per kg body weight), a potent non‐steroidal anti‐inflammatory and antipyretic agent. This agent, however, only had a partial antagonistic influence upon pyrogen‐induced ruminal stasis. The secondary changes in heart rate were not prevented by the drug. It seems unlikely that the inhibition of the extrinsic ruminal contractions by exogenous pyrogens is due simply to a release of prostaglandins.

A comparison of the role of kinins and serotonin in endotoxin induced fever and Trypanosoma vivax infections in the goat

Goats were infected with Trypanosoma vivax or inoculated with a low pyrogenic dose of lipopolysaccharide (LPS) obtained from Escherichia coli or Salmonella typhimurium in order to obtain evidence about the role of kinins and serotonin in the pathogenesis of trypanosomiasis and in endotoxin induced ruminal stasis. The following conclusions were made: (1) whole blood serotonin and bradykinin-like activity levels and clinical symptoms during fever, induced by LPS E coli or T vivax infection are not comparable. (2) There is no good correlation between the changes in heart rate and the temperature rise during fever, evoked by LPS E Coli or T vivax infection. (3) No change of whole blood serotonin level was found during LPS induced fever and only a small increase in the whole blood bradykinin-like activity could be detected. These data suggest that the inhibition of the extrinsic ruminal contractions and the bradycardia followed by a biphasic increase in heart rate during LPS induced fever are not mediated by these substances. (4) The peaks of parasitaemia during the acute phase of T vivax infection are associated with increases in whole blood bradykinin level. However, the high blood bradykinin-like activity did not cause an inhibition of the extrinsic ruminal contractions. (5) The slightly raised bradykinin-like activity during the chronic phase of T vivax infection suggests that bradykinin is not a major factor in the pathogenesis of chronic T vivax infection. (6) The fluctuations of the blood serotonin level during temperature peaks, associated with peaks of parasitaemia and the presence of many platelet thrombi in goats dying during overwhelming parasitaemia suggests a correlation between T vivax, platelet aggregation and blood serotonin decrease.

An evaluation of ammonium sulphate as a potential NPN source for ruminants

Experiments were undertaken to examine the comparative toxicity to sheep of ammonium sulphate and urea given as single doses and the value of ammonium sulphate fed alone or in combination with urea as a supplement to low nitrogen roughages. Ammonium sulphate dosing produced significantly lower mean blood ammonia levels than urea dosing. Fifteen grams of nitrogen as ammonium sulphate were tolerated as a single dose but the equivalent level of urea was toxic. lnappetance and ruminal stasis was noted when sheep fed a low nitrogen roughage (0.5 per cent nitrogen) received ammonium sulphate supplement as the sole non-protein nitrogen source. Ruminal stasis and inappetance may have been due to sulphide toxicity. Ammonium sulphate when used at lower levels in varying combinations with urea was well utilized as a nitrogen and sulphur source even when supplying 50 per cent of the supplemented nitrogen.