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      Small doses of epinephrine prolong the recovery from a rocuronium-induced neuromuscular block: a case report

      case-report
      BMC Anesthesiology
      BioMed Central
      Catecholamines, Epinephrine, Neuromuscular blocking agents, Rocuronium

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          Abstract

          Background

          During anaesthesia it is not uncommon to administer epinephrine in patients blocked by non-depolarizing muscle relaxants. However, there are few reports on possible interaction of epinephrine with neuromuscular transmission in humans.

          Case presentation

          An otherwise healthy 74-yr-old man underwent transurethral resection of a benign prostatic hyperplasia under total intravenous anaesthesia. Because of repeated drop in heart rate and blood pressure the patient received in total three bolus of epinephrine 5 μg, respectively. Each time this small dose of epinephrine intensified a rocuronium-induced neuromuscular block verified by acceleromygraphy. Further anaesthetic course was uneventful.

          Conclusions

          In this case reported here small doses of intravenously administered epinephrine markedly prolonged a rocuronium-induced neuromuscular block. Given the widely used co-administration of epinephrine and muscle relaxants possible adrenergic interference with neuromuscular transmission would have implications for daily anaesthetic practice.

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          Most cited references14

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          Role of the newer alpha, -adrenergic-receptor antagonists in the treatment of benign prostatic hyperplasia-related lower urinary tract symptoms.

          Although initially introduced for the management of hypertension, alpha(1)-adrenergic-receptor antagonists (alpha1-blockers) have become the standard of care for the medical management of benign prostatic hyperplasia (BPH)-related lower urinary tract symptoms (LUTS). However, these agents have the potential to produce orthostatic hypotension and other blood pressure-related adverse effects in normotensive patients and in those receiving concurrent treatment with other antihypertensive agents. As a result, more "uroselective," less vasoactive alpha(1)-blockers have been developed. This article reviews current information on the role of alpha(1)-blockers in the treatment of BPH-related LUTS. The focus is on tamsulosin and alfuzosin, newer "uroselective" agents in this class that have a decreased potential for cardiovascular adverse effects. Relevant articles were identified through a search of the English-language literature indexed on MEDLINE and the proceedings of scientific meetings from 1976 to 2003. The search terms were benign prostatic hyperplasia treatment, alpha(1)-adrenergic-receptor blocker, uroselectivity, lower urinary tract symptoms, complications, and cardiovascular. Tamsulosin has selectivity for the a alpha(1) and alpha(1d) receptor subtypes. Alfuzosin, although not receptor subtype selective, is clinically "uroselective" and does not significantly affect vascular alpha-adrenergic receptors. Both agents are efficacious in relieving LUTS and have a decreased potential for such cardiovascular adverse effects as postural hypotension. Common adverse events with these agents include dizziness and asthenia. Based on the available data, "uroselective" alpha(1)-blockers should be considered over older, more vasoactive agents for the medical management of LUTS, particularly in patients with BPH and hypertension.
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            Onset and duration of action of rocuronium--from tracheal intubation, through intense block to complete recovery.

            The primary objective of this study was to establish the relation between the post tetanic count (PTC) and the time to reappearance of the first response (T1) in train-of-four (TOF) nerve stimulation following rocuronium 0.6 mg/kg, 0.9 mg/kg, and 1.2 mg/kg. The secondary objective was to evaluate the intubation conditions after 1 min.
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              ATP released together with acetylcholine as the mediator of neuromuscular depression at frog motor nerve endings.

              1. The hypothesis that ATP released by presynaptic stimulation is hydrolysed to adenosine and mediates prejunctional neuromuscular depression was tested at vertebrate neuromuscular junctions. Electrophysiological recordings of evoked acetylcholine (ACh) release and perineural ionic currents at motor nerve endings were made using the frog cutaneous pectoris nerve-muscle preparation. Either tubocurarine or alpha-bungarotoxin was used to block muscle contractions. 2. Either alpha,beta-methylene ADP (which inhibits ecto-5'nucleotidases and thus prevents the degradation of ATP to adenosine) or selective adenosine receptor antagonists (8-cyclo-pentyl alkyl xanthines) prevented the inhibitory effects of exogenous ATP on ACh release in response to low-frequency nerve stimulation. These results confirm earlier findings that ATP must be hydrolysed to adenosine to inhibit ACh release. 3. The presence of alpha,beta-methylene ADP completely prevented neuromuscular depression in response to repetitive high-frequency nerve stimulation (0.5-1 Hz). alpha,beta-Methylene ADP had no effect on ACh secretion under conditions where ACh release is well maintained (low-frequency stimulation, 0.05 Hz). 4. Selective adenosine receptor antagonists completely eliminated neuromuscular depression produced by repetitive high-frequency nerve stimulation (1.0 Hz) but had no effect on ACh release at low frequencies of stimulation (0.05 Hz). 5. Exogenous adenosine deaminase (5 i.u. ml-1), which degrades adenosine to its inactive nucleoside inosine, also eliminated neuromuscular depression but had no significant effect on ACh release at frequencies of nerve stimulation too low to produce prejunctional depression. 6. During maximal neuromuscular depression, the effects of exogenous adenosine or 2-chloroadenosine, an adenosine agonist, were occluded. 7. The calcium-sensitive component of perineurial recordings of motor nerve terminal currents did not change during depression or during application of adenosine receptor antagonists and adenosine deaminase, suggesting that neuromuscular depression in this species was not associated with changes in presynaptic Ca2+ currents. 8. These results suggest that, under the conditions of these experiments, endogenous ATP, after hydrolysis to adenosine, causes prejunctional neuromuscular depression. This inhibitory effect of endogenous adenosine occurs at a site distal to the locus of Ca2+ entry in the frog.
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                Author and article information

                Contributors
                hubert.schmitt@kfa.imed.uni-erlangen.de
                Journal
                BMC Anesthesiol
                BMC Anesthesiol
                BMC Anesthesiology
                BioMed Central (London )
                1471-2253
                11 July 2018
                11 July 2018
                2018
                : 18
                : 82
                Affiliations
                ISNI 0000 0001 2107 3311, GRID grid.5330.5, Department of Anaesthesia, , Friedrich-Alexander University Erlangen-Nuremberg, ; Krankenhausstrasse 12, D-91054 Erlangen, Germany
                Author information
                http://orcid.org/0000-0003-0804-4289
                Article
                544
                10.1186/s12871-018-0544-2
                6042291
                29996773
                2cdeb624-69df-498c-98d2-a8a1b1624c5d
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 8 November 2017
                : 20 June 2018
                Categories
                Case Report
                Custom metadata
                © The Author(s) 2018

                Anesthesiology & Pain management
                catecholamines,epinephrine,neuromuscular blocking agents,rocuronium

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