Buprenorphine given intravenously (6 μg kg−1) was examined for its antinociceptive activity in unrestrained sheep using devices to measure thermal and mechanical thresholds The plasma levels of buprenorphine following intravenous injection over the time period of the antinociceptive testing were measured using a radioimmunoassay. Buprenorphine produced a clear antinociceptive effect lasting for up to three and a half hours when measured by the thermal threshold test, but no detectable antinociception in the mechanical test. The plasma levels of buprenorphine indicated that the drug was rapidly distributed in a manner not dissimilar to that reported in man, although individual animals showed a wide variation in some parameters. When plasma levels of the drug were high (< 700 pg ml−1) during the first sixty minutes, no antinociceptive activity in the thermal test could be detected, which may be due to the slow receptor kinetics shown by this drug.

No abstract

Threshold responses were measured to a thermal skin test and a mechanical pressure test in two groups of conscious unrestrained sheep. The first group of sheep were healthy adult females and formed a control sample, the second group were also adult females, but were all suffering from a condition known as footrot. Footrot is a chronic infective lesion affecting usually one foot which appears to cause severe pain in its worst manifestation. These sheep were assessed for the severity of the lesion and degree of lameness and were divided into high and low severity subgroups. Footrot did not alter the threshold to the thermal test but the mechanical pressure threshold was significantly reduced in both footrot sub-groups compared to controls. A local anaesthetic block of the affected foot restored values to close to the control level. After treatment of the affected foot, the mechanical threshold in the low severity sub-group was returned to normal, but in the high severity sub-group it was still significantly reduced compared to the control animals. However, when retested 3 months later these values had returned to the normal control levels.

No abstract

Xylazine and clonidine, given intravenously, cause an increase in airway pressure in the anaesthetized, ventilated sheep. This increase was dose dependent and was not mediated by histamine, nor was it blocked by the alpha 1-adrenoceptor antagonist prazosin. However, the increase was abolished by the alpha 2-adrenoceptor antagonist, idazoxan. When the alpha 2-adrenoceptor agonists were administered into the cerebrospinal fluid by injection into the cisterna magna there was no increase in airway pressure, although a similar dose given peripherally still produced an effect. These findings would indicate that the increase in airway pressure seen in these sheep, following administration of xylazine and clonidine, was mediated by peripherally located alpha 2-adrenoceptors.