{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T06:40:56Z","timestamp":1778568056125,"version":"3.51.4"},"reference-count":30,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2018,6,16]],"date-time":"2018-06-16T00:00:00Z","timestamp":1529107200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000361","name":"Diabetes UK","doi-asserted-by":"publisher","award":["BDA\/RD:06\u22120003255"],"award-info":[{"award-number":["BDA\/RD:06\u22120003255"]}],"id":[{"id":"10.13039\/501100000361","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabet. Med."],"published-print":{"date-parts":[[2018,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Hypoglycaemia causes <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content>\u2010interval prolongation and appears pro\u2010arrhythmogenic. Salbutamol, a \u03b2<jats:sub>2<\/jats:sub>\u2010adrenoreceptor agonist also causes <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content>\u2010interval prolongation. We hypothesized that the magnitude of electrophysiological changes induced by salbutamol and hypoglycaemia might relate to each other and that salbutamol could be used as a non\u2010invasive screening tool for predicting an individual's electrophysiological response to hypoglycaemia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Eighteen individuals with Type 1 diabetes were administered 2.5 mg of nebulized salbutamol. Participants then underwent a hyperinsulinaemic\u2013hypoglycaemic clamp (2.5 mmol\/l for 1 h). During both experiments, heart rate and serum potassium (and catecholamines during the clamp) were measured and a high\u2010resolution electrocardiogram (<jats:styled-content style=\"fixed-case\">ECG<\/jats:styled-content>) was recorded at pre\u2010set time points. Cardiac repolarization was measured by <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content>\u2010interval duration adjusted for heart rate (<jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content><jats:sub>c<\/jats:sub>), T\u2010wave amplitude (T<jats:sub>amp<\/jats:sub>), T\u2010peak to T\u2010end interval duration (T<jats:sub>p<\/jats:sub>T<jats:sub>end<\/jats:sub>) and T\u2010wave area symmetry (T<jats:sub>sym<\/jats:sub>). The maximum changes vs. baseline in both experiments were assessed for their linear dependence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Salbutamol administration caused <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content><jats:sub>c<\/jats:sub> and T<jats:sub>p<\/jats:sub>T<jats:sub>end<\/jats:sub> prolongation and a decrease in T<jats:sub>amp<\/jats:sub> and T<jats:sub>sym<\/jats:sub>. Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content><jats:sub>c<\/jats:sub> and T<jats:sub>p<\/jats:sub>T<jats:sub>end<\/jats:sub> prolongation, and a decrease in T<jats:sub>amp<\/jats:sub> and T<jats:sub>sym<\/jats:sub>. No significant correlations were found between maximum changes in <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content><jats:sub>c<\/jats:sub> [<jats:italic>r<\/jats:italic> = 0.15, 95% confidence interval (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>) \u22120.341 to 0.576; <jats:italic>P<\/jats:italic> = 0.553), T<jats:sub>p<\/jats:sub>T<jats:sub>end<\/jats:sub> (<jats:italic>r<\/jats:italic> = 0.075, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> \u22120.406 to 0.524; <jats:italic>P<\/jats:italic> = 0.767), T<jats:sub>sym<\/jats:sub> (<jats:italic>r<\/jats:italic> = 0.355, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> \u22120.132 to 0.706; <jats:italic>P<\/jats:italic> = 0.149) or T<jats:sub>amp<\/jats:sub> (<jats:italic>r<\/jats:italic> = 0.148, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> \u22120.347 to 0.572; <jats:italic>P<\/jats:italic> = 0.558) in either experiment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Both hypoglycaemia and salbutamol caused pro\u2010arrhythmogenic electrophysiological changes in people with Type 1 diabetes but were not related in any given individual. Salbutamol does not appear useful in assessing an individual's electrophysiological response to hypoglycaemia.<\/jats:p><\/jats:sec>","DOI":"10.1111\/dme.13650","type":"journal-article","created":{"date-parts":[[2018,4,23]],"date-time":"2018-04-23T08:56:29Z","timestamp":1524473789000},"page":"1264-1272","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Salbutamol\u2010induced electrophysiological changes show no correlation with electrophysiological changes during hyperinsulinaemic\u2013hypoglycaemic clamp in young people with Type 1 diabetes"],"prefix":"10.1111","volume":"35","author":[{"given":"P.","family":"Novodvorsky","sequence":"first","affiliation":[{"name":"Department of Oncology and Metabolism University of Sheffield"},{"name":"Sheffield Teaching Hospitals NHS Foundation Trust"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Bernjak","sequence":"additional","affiliation":[{"name":"Department of Oncology and Metabolism University of Sheffield"},{"name":"INSIGNEO Institute for in silico Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. J.","family":"Robinson","sequence":"additional","affiliation":[{"name":"Department of Oncology and Metabolism University of Sheffield"},{"name":"Sheffield Teaching Hospitals NHS Foundation Trust"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Iqbal","sequence":"additional","affiliation":[{"name":"Department of Oncology and Metabolism University of Sheffield"},{"name":"Sheffield Teaching Hospitals NHS Foundation Trust"},{"name":"Department of Infection, Immunity and Cardiovascular Disease University of Sheffield Sheffield"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I. A.","family":"Macdonald","sequence":"additional","affiliation":[{"name":"School of Life Sciences University of Nottingham Nottingham"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6710-5403","authenticated-orcid":false,"given":"R. M.","family":"Jacques","sequence":"additional","affiliation":[{"name":"School of Health and Related Research University of Sheffield Sheffield UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. L. B.","family":"Marques","sequence":"additional","affiliation":[{"name":"Department of Oncology and Metabolism University of Sheffield"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. J.","family":"Sheridan","sequence":"additional","affiliation":[{"name":"Sheffield Teaching Hospitals NHS Foundation Trust"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2425-9565","authenticated-orcid":false,"given":"S. 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