CGA-72662—A new sheep blowfly insecticide

SUMMARY The efficiency of 2-cyclopropylamino-4, 6-diamino-s-triazine CGA-72662 (proposed common name: cyromazine) for the control of blowfly strike was tested in fly cage and field trials on sheep. The safety to sheep and physico-chemical properties of the compound as they relate to blowfly control were also assessed.     

Reactivity of Equine Palmar Digital Arteries and Veins to Vasodilating Agents

Palmar digital arteries and veins removed surgically from healthy horses under general anesthesia were cut into 4 mm vascular rings, suspended in tissue baths, and attached to force displacement transducers for continuous measurement of vascular tension. In vitro vascular responses were determined for acetylcholine, acepromazine, isoxsuprine hydrochloride (isoxsuprine), prostaglandin E₂ (PGE₂), and prostaglandin I₂ (prostacyclin). After preconstriction with norepinephrine hydrochloride (norepinephrine), or prostaglandin F₂ alpha (PGF₂ alpha), the concentrations needed to produce 50% maximum relaxation (EC₅₀) and the maximum percentage of relaxation were determined for each drug.
Acetylcholine was the most potent arterial vasodilator (smallest EC₅₀ value) and PGE₂ was the least potent. Prostacyclin was the least potent venodilator (highest EC₅₀ value); there were no differences between acetylcholine, acepromazine, isoxsuprine, and PGE₂. Isoxsuprine produced greater arterial relaxation than all other agents. Isoxsuprine and acepromazine produced significantly greater venous relaxation than did acetylcholine and PGE₂. Prostacyclin produced minimal vasodilation of arteries or veins. Acepromazine and isoxsuprine relaxed the veins significantly more than the arteries. When PGF₂ alpha was used instead of norepinephrine to preconstrict the arteries and veins, the potency and effectiveness of acepromazine and isoxsuprine to produce vasodilation were significantly decreased. Results indicate that acepromazine and isoxsuprine can relax the equine digital vasculature but their effectiveness varies depending on the origin of the constriction.     

Intraoperative Monitoring of Ischiatic Nerve Function with Sensory Evoked Potentials

Serial recordings of sensory evoked potentials (SEP) generated in response to stimulation of each tibial nerve were obtained from 23 anesthetized dogs. Five dogs were anesthetized for 3 hours to evaluate changes in serial SEP during general anesthesia. Nonsurgical and surgical manipulations were performed on one hind limb of five dogs to determine the effects of limb positioning and nerve retraction on SEP. In 13 dogs, the ischiatic nerve was exposed surgically and retracted until the SEP deteriorated and disappeared, to determine the relationship between amount of tension on the nerve and the time to complete deterioration of the SEP. Sensory evoked potential waveforms, which consisted of two to five peaks, were stable throughout the anesthetic period. The first two peaks were the most stable. Latency of the first two peaks was the easiest and most reliable parameter to evaluate. Although the peak latency in recordings from the superior hind limb was always slightly longer, SEP recordings from the inferior limb were good controls to monitor nerve function. There was considerable variation in sensitivity to nerve retraction. The technique proved to be a reliable way to monitor nerve function in normal anesthetized dogs.     

Haemobartonellosis in a dog

SUMMARY Haemobartonella canis was identified in the peripheral blood of a splenectomised dog with a regenerative anaemia. Treatment with tetracycline and prednisolone led to remission of the parasitaemia and increase in the packed cell volume. Mild parasitaemia was again observed when the dog was clinically normal.     

Quantitative electroencephalography for measurement of central nervous system responses to diazepam and the benzodiazepine antagonist, flumazenil, in isoflurane-anaesthetized dogs

Quantitative EEG was assessed in six dogs anaesthetized with 1.8% end-tidal isoflurane concentration and following diazepam (0.2 mg/kg i.v.) administration. Ventilation was controlled to maintain normocapnia. Five dogs were subsequently given the benzodiazepine antagonist, flumazenil (0.04 mg/kg i.v.), and quantitative EEG was recorded. One dog received a saline injection following diazepam (as a control) and quantitative EEG was recorded for an additional 2.5 h. Heart rate, arterial blood pressure, esophageal temperature, arterial pH and blood gas tensions, end-tidal CO2 tension and end-tidal isoflurane concentration were monitored throughout the study. A 21 lead linked-ear montage was used for recording EEG. Quantitative EEG data were stored on an optical disc for analysis at a later date. Values for absolute power of EEG were determined for theta, delta, alpha, and beta frequencies. Cardiovascular parameters remained stable throughout the study. Diazepam administration was associated with decreased absolute power in all frequencies of EEG at all electrode sites. The duration of diazepam-induced decreased absolute power of EEG was at least 3 h in one dog. Administration of flumazenil antagonized diazepam-induced decreased absolute power of EEG in all frequencies at all electrode sites. We conclude that quantitative EEG provides a relatively non-invasive, objective measure of diazepam- and flumazenil-induced changes in cortical activity during isoflurane anaesthesia.