Sedative and cardiorespiratory effects of dexmedetomidine alone or combined with acepromazine in healthy cats.

The purpose of this study was to assess sedation, emesis and cardiovascular effects of dexmedetomidine alone or combined with acepromazine in healthy cats. Fourteen male cats aged 0.9 ± 0.5 years and weighing 3.7 ± 0.7 kg were randomly assigned to one of two experimental groups: GD, dexmedetomidine 5 µg/kg; and GDA, dexmedetomidine 5 µg/kg with acepromazine 0.03 mg/kg, all intramuscularly. Measurements were recorded at baseline, at 20 minutes and then at 10-minute intervals following sedation and included heart rate (HR), respiratory rate (FR), systolic arterial pressure (SAP), rectal temperature (RT), number of episodes of emesis and sedation score (0-4). Data were compared using ANOVA for repeated measures followed by Sídák and Dunnet test. Sedation scores were compared between groups at T20 using Mann-Whitney test. Significance was considered when P <0.05. At T20, HR was significantly lower in GDA (99 ± 14 beats/min) compared with GD (133 ± 19 beats/min) and SAP was significantly lower in both groups compared with baseline (126 ± 14 vs. 148 ± 26 and 111 ± 13 vs. 144 ± 17 mmHg in GD and GDA, respectively). Duration of sedation was similar between groups, although sedation scores differed significantly at T20, with 1 (0-4) in GD and 4 (4-4) in GDA. More episodes of emesis were recorded in GD compared with GDA. The combination of dexmedetomidine and acepromazine produced more profound sedation with faster onset and lower incidence of emesis compared with dexmedetomidine alone in healthy cats.

Gallic acid prevents ketamine-induced oxidative damages in brain regions and liver of rats.

INTRODUCTION: Ketamine (KET) is an anesthetic agent widely used in human and veterinary medicine. According to studies, KET is associated to direct neutorotoxic damages due to its capacity to induce oxidative stress. Because of the free radical generation in the organism and its relation with diseases' development, there is a growing interest to study antioxidant molecules, such as gallic acid (GA), a natural phenolic compound. AIM: Evaluate the GA antioxidant potential for the prevention of oxidative damage in the brain and liver tissue of rats exposed to acute KET administration. MATERIAL AND METHODS: 32 Wistar male rats received GA (by gavage, 13.5 mg/kg) for three consecutive days, 24 h after the last GA dose, animals were anesthetized with KET (50 mg/kg, i.m.). All animals were euthanized by decapitation 60 min after KET administration. The liver, brain cortex and hippocampus were removed and homogenized for biochemical analysis. RESULTS: In brain cortex, KET increased reactive species (RS) generation, protein carbonyls (PC) levels and reduced non-protein thiols (NPSH) levels, while GA pre-treatment reduced PC and increased NPSH levels. KET increased PC and decreased NPSH levels in the hippocampus, and GA reduced PC and NPSH levels. In the liver, no difference was observed in the RS generation, while KET induced and increase of PC levels and decreased NPSH levels, while GA pre-treatment prevented it. CONCLUSION: GA administration can prevent oxidative damage caused by acute KET administration and minimize its noxious effects. Further studies are needed to evidence GA antioxidant properties regarding KET chronic use.

Peripheral perfusion index does not accurately reflect hypoperfusion in healthy dogs undergoing elective ovariohysterectomy.

This study evaluated the variability of the peripheral perfusion index (PI) in 22 anaesthetised female dogs undergoing elective ovariohysterectomy and examined the relationship between peripheral PI and heart rate, blood pressure, blood pH, end tidal CO2 (EtCO2), O2 saturation (SpO2), core-peripheral temperature gradient (ΔTc-p), partial pressure of CO2 (PCO2), and concentrations of glucose, cortisol, lactate and bicarbonate (HCO3-). Blood pH, lactate and glucose concentrations were determined 15, 30, 45min into the ovariohysterectomy procedure and after extubation. Cortisol concentrations were assessed before anaesthesia and after extubation. Other variables were recorded at every 5min throughout the ovariohysterectomy procedure. Hyperglycaemia was observed in 59% of bitches during surgery, but serum cortisol concentrations remained unchanged. Most measures of perfusion (ΔTc-p, pH, PCO2, EtCO2, SpO2) and heart rate remained unchanged throughout anaesthesia and did not correlate with peripheral PI. Mean arterial pressure increased during the ovariohysterectomy procedure, while peripheral PI decreased, resulting in negative correlations between these variables at 30 and 45min. Lactate concentrations decreased from baseline to the time of measurement post-extubation. Peripheral PI gradually decreased during the ovariohysterectomy procedure, probably reflecting vasoconstriction induced by nociceptive stimuli. Using lactate concentrations as the reference standard for peripheral perfusion, low peripheral PI in healthy bitches undergoing ovariohysterectomy might not represent peripheral hypoperfusion.