Arterial baroreflex control of heart rate in the horse, pig, and calf

The heart rate (HR) response to stepwise changes in mean arterial pressure (MAP) produced by methoxamine and sodium nitroprusside was studied in conscious horses, pigs, and calves. The respective steady-state arterial baroreflex sensitivities (delta HR/delta MAP expressed as beats min-1 . mm of Hg-1) were -1.20, -1.21, and -0.39 for decreasing MAP and -0.08, -0.91, and -0.56 for increasing MAP. After parasympathetic nervous system (PNS) blockade with atropine, the reflex sensitivity to decreasing MAP in horses and the pigs decreased to -0.62 and -0.65, respectively (P less than 0.05), whereas the sensitivity in calves was not significantly different from the calves' base-line sensitivity (P greater than 0.05). In pigs, the sensitivity to increasing MAP decreased to -0.43 after PNS blockade (P less than 0.05). Horses and calves had a response to small increases in MAP similar to that observed in the absence of PNS blockade. There was no additional change in HR with larger increases in MAP in these 2 species. These responses indicate that varying degrees of mixed PNS and sympathetic nervous system activity changes mediate the baroreflex change in HR seen for increasing and decreasing MAP in pigs and for decreasing MAP in horses. Predominantly PNS activity is responsible for the response to increasing MAP in the horses and calves, whereas predominantly sympathetic nervous system activity is responsible for the response to decreasing MAP in calves. Comparisons were made between the observations in these 3 species and other mammalian species.     

Validation of several types of noxious stimuli for use in determining the minimum alveolar concentration for inhalation anesthetics in dogs and rabbits

OBJECTIVE: To compare 3 types of noxious stimuli applied to various anatomic areas of anesthetized dogs and rabbits for determination of the minimum alveolar concentration (MAC). ANIMALS: 10 dogs and 10 rabbits. PROCEDURE: Dogs were anesthetized with isoflurane and halothane in a randomized order. Rabbits were anesthetized with isoflurane. The MAC was determined by skin incision on the lateral aspect of the chest; clamping of the tail, paw of the forelimb, and paw of the hind limb; and application of electrical current to the oral mucosa (dogs only), forelimb, and hind limb. The MAC was the end-tidal concentration midway between the value permitting and preventing purposeful movement in response to noxious stimuli. RESULTS: In dogs, mean +/- SEM MAC for isoflurane was 1.27 +/- 0.05% for clamping stimuli, 1.36 +/- 0.04% for oral electrical stimulation, 1.35 +/- 0.04% for electrical stimulation to the limbs, and 1.01 +/- 0.07% for surgical incision. The MAC for halothane was 0.97 +/- 0.03% for tail clamping, 0.96 +/- 0.03% for clamping of the limbs, 1.04 +/- 0.03% for electrical stimulation, and 0.75 +/- 0.06% for surgical incision. In rabbits, MAC for isoflurane was 2.08 +/- 0.02% for clamping stimuli, 2.04 +/- 0.02% for electrical stimulation, and 0.90 +/- 0.02% for surgical incision. The MAC for surgical incision was significantly lower than values for the other methods in both species. CONCLUSIONS AND CLINICAL RELEVANCE: Use of electrical current and clamping techniques resulted in similar MAC values. Surgical incision underestimated MAC values in dogs and rabbits.     

Use of a multiplex polymerase chain reaction assay in the antemortem diagnosis of toxoplasmosis and neosporosis in the central nervous system of cats and dogs

OBJECTIVE: To develop a multiplex polymerase chain reaction (PCR) assay for the detection of Toxoplasma gondii and Neospora caninum DNA in canine and feline biological samples. SAMPLE POPULATION; Biological samples from 7 cats with systemic (n = 4) or CNS (3) toxoplasmosis, 6 dogs with neospora- or toxoplasma-associated encephalitis, and 11 animals with nonprotozoal disease. PROCEDURE: Primers for T gondii, N caninum, and the canine ferritin gene (dogs) or feline histone 3.3 gene (cats) were combined in a single PCR assay. The DNA was extracted from paraffin-embedded brain tissue, CSF, or skeletal muscle. The PCR products with positive results were cloned, and sequence identity was confirmed. RESULTS: Of 7 cats and 4 dogs with immunohistochemical or serologic evidence of toxoplasmosis, PCR results were positive for all cats and 3 dogs for T gondii, and positive for T gondii and N caninum for 1 dog. Another dog had negative PCR results for both parasites. Of 2 dogs with immunohistochemical or serologic evidence of neosporosis, PCR results were positive for 1 for N caninum and positive for the other for T gondii. All negative-control samples yielded negative results for T gondii and N caninum on the PCR assay. CONCLUSIONS AND CLINICAL RELEVANCE: Standard tests for toxoplasmosis or neosporosis associated with the CNS rely on serologic, histologic, or immunohistochemical analysis and can be difficult to interpret. The multiplex PCR assay with built-in control reactions could be a complementary clinical tool for the antemortem diagnosis of toxoplasmosis or neosporosis associated with the CNS.     

Efficacy and safety of topical administration of selamectin for treatment of ear mite infestation in rabbits

OBJECTIVE: To evaluate the efficacy and safety of topical administration of selamectin in rabbits naturally infested with Psoroptes cuniculi. DESIGN: Randomized controlled trial. ANIMALS: 48 mixed-breed domestic rabbits with active P. cuniculi mite populations and clinical ear lesions. PROCEDURES: Rabbits were randomly allocated to 1 of 6 treatment groups. On day 0, rabbits in groups 1 and 2 were given vehicle, rabbits in groups 3 and 4 were given selamectin at a dose of 6 mg/kg (2.7 mg/lb), and rabbits in groups 5 and 6 were given selamectin at a dose of 18 mg/kg (8.2 mg/lb). On day 28, rabbits in groups 2, 4, and 6 were given a second dose of vehicle or selamectin. Otoscopic examinations were performed and ear lesion size was measured weekly for 8 weeks. Quantitative viable mite counts were performed on day 56. RESULTS: On days 7 through 56, lesion sizes for all selamectin-treated groups were significantly lower than sizes for control groups; there were no significant differences in lesion sizes among selamectin-treated groups. All rabbits in the 2 control groups had viable adult P. cuniculi mites for the duration of the study, as determined by otoscopic examination, whereas all rabbits in the 4 selamectin-treated groups were free from P. cuniculi mites on days 7 through 56. No adverse reactions associated with selamectin treatment were observed. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that topical application of selamectin at a dose of 6 or 18 mg/kg can completely eliminate mites from rabbits naturally infested with P. cuniculi.     

Differential effects of phosphodiesterase inhibitors on platelet activating factor (PAF)- and adenosine diphosphate (ADP)-induced equine platelet aggregation

Compounds that activate adenylate cyclase, increasing intracellular cyclic adenosine monophosphate (cAMP), inhibit equine platelet aggregation. Cyclic AMP is broken down by phosphodiesterase (PDE) and, in the present study, the effects of theophylline, a nonselective PDE inhibitor, and selective inhibitors of PDE isoenzymes PDE3, PDE4 and PDE5, on equine platelet aggregation in response to platelet activating factor (PAF) and adenosine diphosphate (ADP) have been examined. Theophylline and the PDE3 inhibitors, trequinsin and quazinone, inhibited both PAF and ADP-induced aggregation in a concentration dependent manner. The inhibition of PAF-induced aggregation was, however, significantly greater than that of the response to ADP. The inhibitory effects of theophylline and the PDE3 inhibitors on ADP- but not PAF-, induced aggregation were reversed by addition of the calcium ionophore, A23187. Rolipram and zaprinast, inhibitors of PDE4 and PDE5, respectively, had no effect on either PAF- or ADP-induced aggregation. These results demonstrate that inhibition of aggregation caused by PAF or ADP can be achieved by selective inhibition of PDE3 but suggest that there may be agonist-specific differences in the intracellular signalling pathways that regulate equine platelet aggregation.