To determine whether dobutamine, norepinephrine or phenylephrine infusions alleviate hypotension in isoflurane-anaesthetized dogs administered dexmedetomidine with vatinoxan. Balanced, randomized crossover trial. A total of eight healthy Beagle dogs. Each dog was anaesthetized with isoflurane (end-tidal isoflurane 1.3%) and five treatments: dexmedetomidine hydrochloride (2.5 μg kg^-1) bolus followed by 0.9% saline infusion (DEX-S); dexmedetomidine and vatinoxan hydrochloride (100 μg kg^-1) bolus followed by an infusion of 0.9% saline (DEX-VAT-S), dobutamine (DEX-VAT-D), norepinephrine (DEX-VAT-N) or phenylephrine (DEX-VAT-P). The dexmedetomidine and vatinoxan boluses were administered at baseline (T0) and the treatment infusion was started after 15 minutes (T15) if mean arterial pressure (MAP) was < 90 mmHg. The treatment infusion rate was adjusted every 5 minutes as required. Systemic haemodynamics were recorded at T0 and 10 (T10) and 45 (T45) minutes. A repeated measures analysis of covariance model was used. Most dogs had a MAP < 70 mmHg at T0 before treatment. Treatments DEX-S and DEX-VAT all significantly increased MAP at T10, but systemic vascular resistance index (SVRI) was significantly higher and cardiac index (CI) lower after DEX-S than after DEX-VAT. CI did not significantly differ between DEX-S and DEX-VAT-S at T45, while SVRI remained higher with DEX-S. Normotension was achieved by all vasoactive infusions in every dog, whereas MAP was below baseline with DEX-VAT-S, and higher than baseline with DEX-S at T45. Median infusion rates were 3.75, 0.25 and 0.5 μg kg^-1 minute^-1 for dobutamine, norepinephrine and phenylephrine, respectively. Dobutamine and norepinephrine increased CI (mean ± standard deviation, 3.35 ± 0.70 and 3.97 ± 1.24 L minute^-1 m^-2, respectively) and decreased SVRI, whereas phenylephrine had the opposite effect (CI 2.13 ± 0.45 L minute^-1 m^-2). Hypotension in isoflurane-anaesthetized dogs administered dexmedetomidine and vatinoxan can be treated with either dobutamine or norepinephrine.

Three young grey seals (Halichoerus grypus) were presented separately for fracture repair to the veterinary teaching hospital of University College Dublin. The seals were premedicated with a combination of pethidine, midazolam and atropine; anaesthesia was induced with propofol via the front flipper vein and maintained with sevoflurane or isoflurane in oxygen. One of the seals did not breathe spontaneously after anaesthesia; a cardiac arrest, resulting in death, occurred after several hours of mechanical ventilation. Post-mortem examination revealed a severe lungworm infestation and parasitic pneumonia in this animal. The two other seals recovered uneventfully from anaesthesia.

The retrolaminar block is a regional anaesthetic technique, first developed in humans, in which the local anaesthetic is deposited directly onto the dorsal aspect of the thoracic or lumbar vertebral lamina. This study aims to evaluate the distribution of landmark-guided thoracolumbar retrolaminar injections in greyhound cadavers. Thirteen injections of contrast-dye solution were performed in eight cadavers at the level of the twelfth thoracic vertebra (T12), with either 20 mL (n = 8, high volume, HV) or 10 mL (n = 5, low volume, LV) per site. The spread of the injectate was evaluated through computed tomography and transverse anatomical dissection. The groups were compared using the Mann–Whitney U test. The median (range) of the extent of the spread was 4 (2–5) and 3 (2–4) intervertebral foramina in the LV and HV groups, respectively. The median (range) of the spread along the retrolaminar space was 3 (2–3) retrolaminar segments in the LV and 3 (2–4) in the HV group. Epidural and retroperitoneal spread was identified in seven cadavers. Following landmark-guided retrolaminar injections, the injectate spread both in the retrolaminar and paravertebral spaces, without any obvious association between the volume of injectate and the extent of the spread. Further studies are warranted to determine the clinical efficacy of the technique.