The aim of this prospective, randomized, blinded crossover study was compare the cardiopulmonary and sedative effects of ketamine in combination with acepromazine, diazepam, dexmedetomidine, ...midazolam or xylazine, injected intramuscularly in rabbits, using eight one-year-old male New Zealand rabbits (4.1 ± 0.40 kg). All treatments included ketamine (K; 30 mg/kg) in combination with one of the following: acepromazine 0.5 mg/kg (treatment KA); diazepam 1 mg/kg (KD); dexmedetomidine 0.025 mg/kg (KDex); midazolam 1 mg/kg (KM); or xylazine 3 mg/kg (KX) mixed in the same syringe and injected intramuscularly. Cardiopulmonary variables, blood gases and sedative scores were measured before injection (T0 or baseline) and every 10 min thereafter, over a 60-min period. There were reductions in heart rate, compared with the baseline, at all evaluation times in treatment KX. Treatments KDex, KM and KX presented reductions in respiratory rate at all evaluation times, in comparison with the baseline. There were reductions in mean arterial pressure in KA and KX at times T10-T60 and in PaO2 in KDex, KM and KX at T10-T50. The sedation scores were similar in KA, KDex, KM and KX at T10-T20. Ketamine in combination with acepromazine, dexmedetomidine, midazolam or xylazine promoted similar sedative effects for twenty minutes, but the α2-agonists can promote hypoxemia.
•Ketamine in combination with acepromazine, dexmedetomidine, midazolam or xylazine were analyzed after a single IM injection.•No sedative differences in rabbits after injection of the KA, KDex, KM and KX; more longer in those treated with KA, KDex or KX.•There was significant decrease in oxygenation when dexmedetomidine or xylazine was used.
To evaluate the cardiorespiratory, sedative and antinociceptive effects of dexmedetomidine alone or in combination with methadone, morphine or tramadol in dogs.
Experimental, blinded, randomized, ...crossover study.
Six mixed breed dogs (two males and four females) weighing 10 ± 4 kg.
The animals were randomly divided into four treatments: D (10 μg kg−1 of dexmedetomidine), DM (dexmedetomidine 10 μg kg−1 and methadone 0.5 mg kg−1); DMO (dexmedetomidine 10 μg kg−1 and morphine 0.5 mg kg−1), and DT (dexmedetomidine 10 μg kg−1 and tramadol 2 mg kg−1). The combinations were administered intramuscularly in all treatments. The variables evaluated were heart rate (HR), respiratory rate (fR), rectal temperature (RT), systolic arterial pressure (SAP), sedation scale and pedal withdrawal reflex. These variables were measured at T0 (immediately before the administration of the protocol) and every 15 minutes thereafter until T105.
A decrease in HR and fR occurred in all the treatments compared with T0, but no significant difference was observed between the treatments. The RT decreased from T45 onward in all the treatments. The SAP did not show a difference between the treatments, but in the DT treatment, the SAP was lower at T30 and T45 compared with T0. The D treatment had lower scores of sedation at T15 to T75 compared with the other treatments, and the DMO and DM treatments showed higher scores at T60 and T75 compared with DT.
The treatments with morphine and methadone added to the dexmedetomidine showed higher sedation scores than the control treatment and the treatment with tramadol added to the dexmedetomidine showed no relevant differences in any of the variables evaluated in the study.
Summary
Although evidence is accumulating that hydroxycarbamide decreases mortality among adults with sickle cell disease (SCD), there are no published data regarding the effect of hydroxycarbamide ...on mortality among children. The Paediatric Hydroxycarbamide Program was established to treat children with SCD aged 3–18 years if they met disease severity criteria. Mortality data and clinical/laboratorial effects of hydroxycarbamide were retrospectively collected for the first 9 years of the Program. Mortality among those who received hydroxycarbamide was compared to that of untreated children. Among 1760 subjects, 267 received hydroxycarbamide at a median dose of 20·8 mg/kg/d (range 10–32) for a median of 2 years (range 0·1–6·5). Survival among hydroxycarbamide‐treated children was significantly greater than that among untreated ones (99·5% vs. 94·5%, P = 0·01), due primarily to fewer deaths from acute chest syndrome and infection. Hydroxycarbamide therapy was significantly associated with increases in haemoglobin concentration, fetal haemoglobin, mean corpuscular volume, and reduction in platelet counts, reticulocytes and neutrophils. Toxicity was minimal and predominantly mild reversible neutropenia. Significantly fewer hospitalizations and emergency room visits, and shorter admissions were observed among hydroxycarbamide‐treated subjects, when compared to the 12‐month period prior to treatment initiation. Hydroxycarbamide therapy reduces disease severity and is probably associated with decreased mortality among children with SCD.
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