Alfaxalone induction dose following administration of medetomidine and butorphanol in the dog

ObjectiveTo determine in dogs the effects of medetomidine and butorphanol, alone and in combination, on the induction dose of alfaxalone and to describe the induction and intubation conditions.Study designProspective, randomized, blinded clinical trial.AnimalsEighty-five client-owned dogs (ASA 1 or 2).MethodsSubjects were block randomized to treatment group according to temperament. The treatment groups were: medetomidine 4 μg kg^?1 (M), butorphanol 0.1 mg kg^?1 (B), or a combination of both (MB), all administered intramuscularly. After 30 minutes, a sedation score was assigned, and alfaxalone 0.5 mg kg^?1 was administered intravenously over 60 seconds by an observer who was unaware of treatment group. Tracheal intubation conditions were assessed and, if tracheal intubation was not possible after 20 seconds, further boluses of 0.2 mg kg^?1 were given every 20 seconds until intubation was achieved. Induction dose and adverse events (sneezing, twitching, paddling, excitement, apnoea and cyanosis) were recorded; induction quality and intubation conditions were scored and recorded.ResultsThe mean dose of alfaxalone required for induction was similar for groups M and B: 1.2 ± 0.4 mg kg^?1. The mean dose requirement for group MB (0.8 ± 0.3 mg kg^?1) was lower than groups M and B (p < 0.0001). Induction dose was not influenced by temperament or level of sedation. Induction and intubation scores did not differ between treatment groups. Adverse events were noted in 16 dogs; there was no association with treatment group, temperament or level of sedation.Conclusions and clinical relevanceMedetomidine and butorphanol administered in combination reduce the anaesthetic induction dose of alfaxalone compared to either agent alone. This difference should be taken into account when using this combination of drugs in a clinical setting.     

Antigenic stability of fimbriae of Bacteroides nodosus

Successful vaccination of sheep against footrot and attempts to eradicate the disease depend on there being a limit to the antigenic diversity of the causative bacterium, Bacteroides nodosus. Fimbrial antigenic variation was therefore investigated in vivo, both under conditions of chronic infection and under the pressure of a vaccine-induced immune response, to ascertain whether this represented an obstacle to such goals. Material was available from 5 experiments and although B. nodosus appeared to have undergone changes in its fimbrial antigens in one of these, the possibility that superinfection was responsible for the variation detected could not be ruled out because all sheep in this case were maintained at pasture. Overall, the results provided no evidence of fimbrial antigenic shift in B. nodosus in vivo and in conclusion, the survival of the organism in the sheep's foot, both in long-term natural infection and following vaccination, must therefore be related to factors other than the ability to undergo antigenic variation in order to evade the host's immune response.     

Elevated beta-endorphin in cerebrospinal fluid after electrical brain stimulation: artifact of contrast infusion?

Beta-Endorphin-like immunoreactivity in cerebrospinal fluid was assayed in 11 patients receiving electrical stimulation of the brain for chronic pain. Immunoreactivity increased dramatically after contrast ventriculography prior to stimulation. No further elevations were observed after stimulation. The magnitude and time course of elevations were identical after placement of electrodes either in the thalamus or in the periventricular gray matter. These results suggest that previous findings of stimulation-induced elevation of beta-endorphin-like immunoreactivity in cerebrospinal fluid are attributable to an artifact of contrast ventriculography.     

Ultrastructure of equine endothelial cells exposed to endotoxin and flunixin meglumine and equine neutrophils

An in vitro system of cultured equine endothelial cells was evaluated as a model for endotoxin (ET) exposure in the horse. Primary cell lines from pulmonary vessels and aortas were cultured from tissues of 6 horses. Effects of ET alone with and without serum and in combination with the cyclo-oxygenase inhibitor flunixin meglumine and isolated equine neutrophils were evaluated by transmission electron microscopy. Cells plus serum were incubated with 10, 25, 50, or 100 micrograms of ET/ml of incubation medium for 1, 3, 8, or 24 hours. Cells without serum were cultured for 1 and 3 hours. Flunixin meglumine was used at a concentration of 20 micrograms/ml. Cells also were incubated in the presence of 1,000, 5,000, or 20,000 neutrophils/ml plus ET and in the presence of a combination of ET and flunixin meglumine for 1 or 3 hours. Endotoxin alone did not cause cell damage, and the only evidence of an effect was an increased number of secondary lysosomes at incubation hour 8. At incubation hour 24, cells appeared normal. Endotoxin plus neutrophils caused cells to become round and detach from the growth substrate. Cell pathologic changes included swollen and distorted mitochondria and cytoplasmic vacuolization. Response to the ET plus neutrophil combination was variable and ranged from 5% to 50% of the cells being affected. The variability appeared to have some correlation with cell age, as well as individual preparation of neutrophils.