{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T20:23:00Z","timestamp":1777666980518,"version":"3.51.4"},"reference-count":28,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[1996,2,1]],"date-time":"1996-02-01T00:00:00Z","timestamp":823132800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[1996,2]]},"abstract":"<jats:p>1 Respiratory and cardiovascular failure are principle toxic effects of \u03b2-blocker overdose. Respiratory arrest is the primary cause of death in \u03b2-blocker intoxicated rats.<\/jats:p>\n                  <jats:p>\n                    2 The effect of \u03b2-adrenoceptor agonists on respiratory and cardiovascular failure in \u03b2-blocker overdose was investigated in a model of acute d,l-propranolol (30 mg kg\n                    <jats:sup>-1<\/jats:sup>\n                    h\n                    <jats:sup>-1<\/jats:sup>\n                    ) intoxication in spontaneously breathing rats.\n                  <\/jats:p>\n                  <jats:p>\n                    3 Neither the aselective, hydrophilic \u03b2-agonist isoprena line (10, 25, 50 \u03bcg kg\n                    <jats:sup>-1<\/jats:sup>\n                    min\n                    <jats:sup>-1<\/jats:sup>\n                    ), nor the \u03b2\n                    <jats:sub>1<\/jats:sub>\n                    -selective, lipophilic \u03b2-agonist flerobuterol (1,3,10 \u03bc g kg\n                    <jats:sup>-1<\/jats:sup>\n                    min\n                    <jats:sup>-1<\/jats:sup>\n                    ) and the \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    -selective, lipophilic \u03b2-agonist clenbuterol (10, 25, 50 \u03bcg kg\n                    <jats:sup>-1<\/jats:sup>\n                    min\n                    <jats:sup>-1<\/jats:sup>\n                    ) had any beneficial effect on cardiovascular and respiratory variables or survival time in d,l-propranolol intoxicated spontaneously breathing rats.\n                  <\/jats:p>\n                  <jats:p>\n                    4 Isoprenaline (10 \u03bcg kg\n                    <jats:sup>-1<\/jats:sup>\n                    min\n                    <jats:sup>-1<\/jats:sup>\n                    ) had no favourable effect on haemodynamic and respiratory variables in artificially ventilated d,l -propranolol intoxicated rats either.\n                  <\/jats:p>\n                  <jats:p>5 Addition of dopamine to isoprenaline resulted in a significant reduction of survival time, primarily caused by a decrease in mean arterial blood pressure, in artificially ventilated d,l-propranolol intoxicated rats. Addition of glucagon to isoprenaline did not affect survival time. 6 Artificial ventilation is the most important supportive measure in d,l-propranolol intoxication in the rat.<\/jats:p>","DOI":"10.1177\/096032719601500204","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T01:08:04Z","timestamp":1230080884000},"page":"120-128","source":"Crossref","is-referenced-by-count":14,"title":["Reduced survival after isoprenaline\/ dopamine in d,l-propranolol intoxicated rats"],"prefix":"10.1177","volume":"15","author":[{"given":"AE","family":"Toet","sequence":"first","affiliation":[{"name":"National Poison Control Centre, National Institute of Public Health and Environmental Protection, Department of Intensive Care and Clinical Toxicology, Utrecht University Hospital, PO Box 85.500, 3508 GA Utrecht, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JD","family":"te 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