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      Analgesic, cardiorespiratory effects and motor block characteristics of epidural levobupivacaine alone or in combination with methadone or dexmedetomidine in bitches undergoing unilateral total mastectomy

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          Abstract

          Abstract The aim of this study was to evaluate the latency, extent of analgesia, and duration of motor block of levobupivacaine alone and combined with methadone or dexmedetomidine after epidural administration during and after mastectomy in dogs. Twenty-four mature, mixed-breed female dogs were randomly divided into three experimental groups with eight animals each, according to the agents used in lumbosacral epidural analgesia: levobupivacaine 0.75% alone (1.5mg/kg - control group), levobupivacaine 0.75% (1.5 mg/kg) + methadone 1% (0.3 mg/kg), or levobupivacaine 0.75% (1.5 mg/kg) + dexmedetomidine 0.05% (3 µg/kg). During surgery, cardiorespiratory parameters were evaluated. Rescue analgesia was given when there were signs of nociception and was necessary in all three treatment groups. Since all animals received rescue analgesia during the surgery and immediately post-surgery, the duration of the sensitive block were not evaluated. The extent of sensory block was between the 12º and 13º thoracic vertebrae for the control group, 7º thoracic vertebra to 5º lumbar vertebra (methadone group), and 8º thoracic vertebra to 4º lumbar vertebra for the dexmedetomidine group. Methadone or dexmedetomidine combined with levobupivacaine increased the extent of the sensory block and the duration of the motor block in bitches when administered via the epidural route.

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          Most cited references49

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          Clinical Pharmacokinetics and Pharmacodynamics of Dexmedetomidine

          Dexmedetomidine is an α2-adrenoceptor agonist with sedative, anxiolytic, sympatholytic, and analgesic-sparing effects, and minimal depression of respiratory function. It is potent and highly selective for α2-receptors with an α2:α1 ratio of 1620:1. Hemodynamic effects, which include transient hypertension, bradycardia, and hypotension, result from the drug’s peripheral vasoconstrictive and sympatholytic properties. Dexmedetomidine exerts its hypnotic action through activation of central pre- and postsynaptic α2-receptors in the locus coeruleus, thereby inducting a state of unconsciousness similar to natural sleep, with the unique aspect that patients remain easily rousable and cooperative. Dexmedetomidine is rapidly distributed and is mainly hepatically metabolized into inactive metabolites by glucuronidation and hydroxylation. A high inter-individual variability in dexmedetomidine pharmacokinetics has been described, especially in the intensive care unit population. In recent years, multiple pharmacokinetic non-compartmental analyses as well as population pharmacokinetic studies have been performed. Body size, hepatic impairment, and presumably plasma albumin and cardiac output have a significant impact on dexmedetomidine pharmacokinetics. Results regarding other covariates remain inconclusive and warrant further research. Although initially approved for intravenous use for up to 24 h in the adult intensive care unit population only, applications of dexmedetomidine in clinical practice have been widened over the past few years. Procedural sedation with dexmedetomidine was additionally approved by the US Food and Drug Administration in 2003 and dexmedetomidine has appeared useful in multiple off-label applications such as pediatric sedation, intranasal or buccal administration, and use as an adjuvant to local analgesia techniques.
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            Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block.

            The purpose of this study was to compare the onset and duration of sensory and motor block, as well as the hemodynamic changes and level of sedation, following intrathecal bupivacaine supplemented with either dexmedetomidine or clonidine. In a prospective, double-blind study, 60 patients undergoing transurethral resection of prostate or bladder tumor under spinal anesthesia were randomly allocated to one of three groups. Group B received 12 mg of hyperbaric bupivacaine, group D received 12 mg of bupivacaine supplemented with 3 microg of dexmedetomidine and group C received 12 mg of bupivacaine supplemented with 30 microg of clonidine. The onset times to reach peak sensory and motor levels, and the sensory and motor regression times, were recorded. Hemodynamic changes and the level of sedation were also recorded. Patients in groups D and C had a significantly shorter onset time of motor block and significantly longer sensory and motor regression times than patients in group B. The mean time of sensory regression to the S1 segment was 303 +/- 75 min in group D, 272 +/- 38 min in group C and 190 +/- 48 min in group B (B vs. D and B vs. C, P < 0.001). The regression of motor block to Bromage 0 was 250 +/- 76 min in group D, 216 +/- 35 min in group C and 163 +/- 47 min in group B (B vs. D and B vs. C, P < 0.001). The onset and regression times were not significantly different between groups D and C. The mean arterial pressure, heart rate and level of sedation were similar in the three groups intra-operatively and post-operatively. Dexmedetomidine (3 microg) or clonidine (30 microg), when added to intrathecal bupivacaine, produces a similar prolongation in the duration of the motor and sensory block with preserved hemodynamic stability and lack of sedation.
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              The hemodynamic and adrenergic effects of perioperative dexmedetomidine infusion after vascular surgery.

              We tested dexmedetomidine, an alpha(2) agonist that decreases heart rate, blood pressure, and plasma norepinephrine concentration, for its ability to attenuate stress responses during emergence from anesthesia after major vascular operations. Patients scheduled for vascular surgery received either dexmedetomidine (n = 22) or placebo (n = 19) IV beginning 20 min before the induction of anesthesia and continuing until 48 h after the end of surgery. All patients received standardized anesthesia. Heart rate and arterial blood pressure were kept within predetermined limits by varying anesthetic level and using vasoactive medications. Heart rate, arterial blood pressure, and inhaled anesthetic concentration were monitored continuously; additional measurements included plasma and urine catecholamines. During emergence from anesthesia, heart rate was slower with dexmedetomidine (73 +/- 11 bpm) than placebo (83 +/- 20 bpm) (P = 0.006), and the percentage of time the heart rate was within the predetermined hemodynamic limits was more frequent with dexmedetomidine (P < 0.05). Plasma norepinephrine levels increased only in the placebo group and were significantly lower for the dexmedetomidine group during the immediate postoperative period (P = 0.0002). We conclude that dexmedetomidine attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia. The alpha(2) agonist, dexmedetomidine, attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia in vascular surgery patients.
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                Author and article information

                Journal
                aabc
                Anais da Academia Brasileira de Ciências
                An. Acad. Bras. Ciênc.
                Academia Brasileira de Ciências (Rio de Janeiro, RJ, Brazil )
                0001-3765
                1678-2690
                2022
                : 94
                : suppl 3
                : e20210082
                Affiliations
                [2] Botucatu São Paulo orgnameUniversidade Estadual Paulista orgdiv1Faculdade de Medicina Veterinária e Zootecnia Brazil
                [1] Campo Grande orgnameUniversidade Federal do Mato Grosso do Sul orgdiv1Faculdade de Medicina Veterinária e Ciência Animal Brazil
                Article
                S0001-37652022000701307 S0001-3765(22)09400001307
                10.1590/0001-3765202220210082
                36477226
                5801dca9-8775-4e59-bad9-dfea8451bed8

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 17 June 2021
                : 27 January 2021
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 49, Pages: 0
                Product

                SciELO Brazil

                Categories
                Animal Science

                analgesia,α-2 agonists,motor block,opioids,sensory block
                analgesia, α-2 agonists, motor block, opioids, sensory block

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