PubMed · 9611444
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L D Carson-Mann. Desquamative gingivitis.. https://pubmed.ncbi.nlm.nih.gov/9611444/
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The plasma pharmacokinetics of doramectin and invermectin after topical administration (500 microg kg(-1)) were compared over a 50-day period in 24 young beef cattle. Observed maximum concentration (Cmax) and time to maximum concentration (Tmax) were determined directly from plasma concentrations for each animal. The area under the plasma concentration-time curve (AUC) and mean residence time (MRT) were calculated as indices of drug exposure and persistence. The Cmax of doramectin (12.2+/-4.8 ng ml(-1)) and ivermectin (12.2+/-6.0 ng ml(-1)) and Tmax of doramectin (4.3+/-1.6 days) and ivermectin (3.4+/-0.8 days) were not significantly different (p > 0.05). In contrast, the AUC of doramectin (168.0+/-41.7 ng day ml(-1)) was significantly greater than that of ivermectin (115.5+/-43.0 ng day ml(-1)). Furthermore, the range of AUC values calculated for ivermectin was wider than that obtained for doramectin, extending from 51.3 to 182.3 ng day ml(-1) for ivermectin versus 104.3-228.7 ng day ml(-1) for doramectin. The MRT was significantly greater for doramectin (12.8+/-1.9 days) than for ivermectin (8.4+/-1.5 days). It was concluded that a 500 microg kg(-1) pour-on administration of doramectin and ivermectin led to an overall exposure as reflected by the mean AUC, that was 45% higher for doramectin compared to ivermectin and that the relative inter-individual variability was less for doramectin than for ivermectin. Possible therapeutic consequences of these differences between doramectin and ivermectin pour-on formulations are discussed.
Capsaicin depletes the sensory neuropeptide substance P (SP) in the rat due to a combination of neuron loss and decreased synthesis in the surviving cells. Resiniferatoxin (RTX) mimics most, but not all, capsaicin actions. In the present study, the effects of RTX (300 microg/kg, s.c.) were examined on mRNA levels for SP and its receptor in the adult rat. The percentage of dorsal root ganglia (DRG) neuronal profiles showing an in situ hybridization signal for preprotachykinin mRNAs encoding SP was not altered following RTX treatment (up to 8 weeks), though the signal became perceptibly weaker. In accord, 2 weeks after RTX administration a 60% decrease was observed in the steady-state levels of SP-encoding mRNAs using Northern blot analysis, leaving the ratio of beta- and gamma-preprotachykinin mRNAs unchanged. No change was, however, observed in mRNA levels encoding tachykinins NK-1 receptors in the dorsal horn, the spinal targets for SP. The present findings suggest that RTX does not kill SP-positive DRG neurons, though it suppresses the synthesis of SP. Since RTX treatment does not alter NK-1 receptor expression, this reduced SP synthesis is likely to play a central role in the analgesic actions of RTX.
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