Search

In conscious sheep, beta-endorphin (1 and 2 micrograms/kg) administered into the third cerebral ventricle caused psychomotor excitability and a significant inhibition of the frequency of rumen contractions. The amplitude of the first rumen contractions, following immediately after the end of endorphin infusion, and the average amplitude of primary rumen contractions were also inhibited. De-efferentiation at the level of the hypothalamus prevented both the inhibitory effect of beta-endorphin on the frequency of rumen contractions and the drug-induced psychomotor excitability. However, de-efferentiation did not prevent beta-endorphin-induced inhibition of the mean amplitude of rumen contractions. The character of pathohistological changes induced by de-efferentiation showed descending degenerative changes of the nerve tracts connecting the hypothalamus with the pons and the medulla oblongata. These results, together with previously published evidence, do suggest that de-efferentiation at the level of the hypothalamus causes degeneration of inhibitory descending opioid-noradrenergic pathways connecting the hypothalamus with the gastric centres in the medulla oblongata.

In sheep, beta-endorphin (1 and 2 micrograms/kg) administered into the third cerebral ventricle caused a significant inhibition of the frequency of rumen contractions. The amplitude of the first rumen contractions, following immediately after the end of infusion, and the average amplitude of primary rumen contractions, were inhibited. Beta-endorphin caused general psychomotor excitability. These results suggest that an inhibitory mu and delta opioid system is involved in the control of forestomach motility and general behaviour in sheep. All effects of beta-endorphin were completely prevented by i.c.v. 6-hydroxydopamine (6-OHDA, 18.2 micrograms/kg) pre-treatment. These results suggest that beta-endorphin-induced inhibition of rumen motility is due to central noradrenergic system activation. The exact location of this noradrenergic system remains to be determined.

When morphine, an opioid mu-agonist, was administered in vivo into the third cerebral ventricle (ICV) of conscious sheep at 20 and 40 micrograms/kg body weight, it caused psychomotor excitability for 2-3 h and a significant decrease in the reticuloruminal frequency for 45 min and in the mean amplitude of the primary contractions for 65 min. From 60 min after infusion, the same doses of morphine caused a significant increase in the average amplitude of the contractions for 45 min. This suggests that an inhibitory mu-opioid acceptor is involved in the central control of forestomach motility and general behaviour in sheep. All the effects of morphine were completely prevented by pretreatment with 18.2 micrograms/kg body weight 6-OHDA ICV. These results suggest that both morphine-induced inhibition of rumen motility and psychomotor excitability are due to central noradrenergic descending system activation. The exact location of the noradrenergic system remains to be determined.

The effect of 60 minutes' intravenous infusions, before morning feeding, of ammonium acetate (18.6 micromole/min/kg of body weight) and ammonium acetate with propranolol (11 microgram/min/kg of body weight) on the ruminal motility of sheep was examined. Ammonia has a adrenaline-like action therefore propranolol, a beta-receptor blocking agent, was administered in order to eliminate the possible effect of adrenaline on ruminal motility. The contractions of the dorsal sack of the rumen were registered by means of the balloon method, with the gauge inserted through the rumen fistula. The infusion of ammonium acetate caused an increase of the ammonia concentration in the blood to 0.6 mmol/1 at the end of 60 minutes' infusion. Already during the first 5 minutes of the intravenous infusion of ammonium acetate there was a decreased frequency of ruminal contractions, which was observed throughout the infusion. After the infusion there was a radical decrease of the concentration of ammonia in the blood, and at the same time an increase in the frequency of rumen contraction was observed. Blocking of the beta-adrenergic receptors by propranolol did not eliminate the inhibiting action of ammonium ion on rumen motility. The infusion of the ammonium acetate caused an increase of adrenaline and glucose concentration. This response was eliminated by propranolol in the case of adrenaline but not glucose. It is assumed that the action of ammonium ion on the rumen motility is derived primarily by the central nervous system.

Pharmacodynamical analysis of alpha-adrenergic and beta-adrenergic reactions of sheep rumen was performed in vivo after administration of agonists and antagonists of alpha-adrenergic and beta-adrenergic receptors. It was found that phenylephrine, and in a lower degree propranolol, stimulated the motor activity of sheep rumen, while adrenaline, noradrenaline, isoprenaline, phenoxybenzamine and regitine depressed this activity. Propranolol abolished atonia produced by catecholamines in sheep rumen, and previous blockade of beta-adrenergic receptors with propranolol reversed the relaxing action of catecholamines on the muscular elements in the rumen. The experiments in vivo confirmed the adrenergic effects on the motor activity of the rumen of sheep obtained in earlier investigations on isolated muscles of the rumen. It is suggested that noradrenaline exerts an ambireceptro effect (similar to that of adrenaline) on the motor activity in sheep rumen.

The alpha and beta-adrenergic responses of the isolated muscle of sheep rumen were analysed by pharmacodynamic methods after administration of alpha and beta-adrenergic agonists and alpha and beta-adrenergic antagonists. It was found that phenylephrine, and in a lower degree propranolol, stimulated contractions of isolated muscle of sheep rumen while adrenaline, noradrenaline, isoprenaline, phenoxybenzamine and regitine inhibited these contractions. Propranolol abolished the dilating (atonic) effect of catecholamines on the isolated muscles of sheep rumen and previous blockade of beta-adrenergic receptors with propranolol reversed the dilating effects of catecholamines. It is concluded that noradrenaline has an ambiceptor effect (similar to that of adrenaline) on the isolated muscle of the rumen.