{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T14:31:07Z","timestamp":1761489067863,"version":"3.38.0"},"reference-count":17,"publisher":"American Veterinary Medical Association (AVMA)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["javma"],"published-print":{"date-parts":[[2013,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n<jats:p><jats:bold>Objective<\/jats:bold>\u2014To compare the cardiorespiratory effects of IM administration of dexmedetomidine-buprenorphine (DB) and dexmedetomidine-buprenorphine-ketamine (DBK) in dogs with subsequent reversal with atipamezole.<\/jats:p>\n<jats:p><jats:bold>Design<\/jats:bold>\u2014Prospective, randomized crossover study.<\/jats:p>\n<jats:p><jats:bold>Animals<\/jats:bold>\u20145 healthy dogs.<\/jats:p>\n<jats:p><jats:bold>Procedures<\/jats:bold>\u2014Dogs were instrumented for cardiac output (CO) measurement and received DB (15 \u03bcg of dexmedetomidine\/kg [6.8 \u03bcg\/lb] and 40 \u03bcg of buprenorphine\/kg [18.2 \u03bcg\/lb]) or DBK (DB plus 3 mg of ketamine\/kg [1.36 mg\/lb]) in randomized order while breathing room air. Atipamezole (150 \u03bcg\/kg [68.2 \u03bcg\/lb], IM) was administered 1 hour later. Hemodynamic data were collected in the conscious dogs and then at 5, 10, 15, 20, 30, 45, and 60 minutes after drug administration. Lactate concentration was measured in mixed venous blood samples. Oxygen delivery (D<jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub>) and oxygen consumption (<jats:inline-formula><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"javma.242.3.339.Vdot.gif\" mimetype=\"image\" xlink:type=\"simple\"\/><\/jats:inline-formula><jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub>) were calculated.<\/jats:p>\n<jats:p><jats:bold>Results<\/jats:bold>\u2014Heart rate (HR), CO, and D<jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub> decreased after DB and DBK administration. The <jats:inline-formula><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"javma.242.3.339.Vdot.gif\" mimetype=\"image\" xlink:type=\"simple\"\/><\/jats:inline-formula><jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub> did not change in the DB group but decreased in the DBK group. The HR was higher in the DBK group than in the DB group throughout the study, but the CO, D<jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub>, and <jats:inline-formula><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"javma.242.3.339.Vdot.gif\" mimetype=\"image\" xlink:type=\"simple\"\/><\/jats:inline-formula><jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub> values were similar for the 2 groups. Blood lactate concentrations remained low (&lt; 1 mmol\/L) throughout the study. Arterial hypoxemia and hypercapnea occurred in both groups. Mean arterial blood pressure and pulmonary artery wedge pressure were markedly increased in both groups, but to a greater extent in the DBK group. After atipamezole administration, HR, CO, and D<jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub> returned to the baseline values.<\/jats:p>\n<jats:p><jats:bold>Conclusions and Clinical Relevance<\/jats:bold>\u2014Adding ketamine to the DB combination allowed dogs to maintain a higher HR and delayed the onset of sinus arrhythmias but failed to provide a significantly higher CO because of a reduction in stroke volume.<\/jats:p>","DOI":"10.2460\/javma.242.3.339","type":"journal-article","created":{"date-parts":[[2013,1,17]],"date-time":"2013-01-17T14:24:38Z","timestamp":1358432678000},"page":"339-345","source":"Crossref","is-referenced-by-count":7,"title":["Influence of ketamine on the cardiopulmonary effects of intramuscular administration of dexmedetomidine-buprenorphine with subsequent reversal with atipamezole in dogs"],"prefix":"10.2460","volume":"242","author":[{"given":"Jeff C.","family":"Ko","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michele","family":"Barletta","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ismail","family":"Sen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann B.","family":"Weil","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebecca A.","family":"Krimins","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark E.","family":"Payton","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Constable","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1272","reference":[{"key":"ref1","series-title":"Drugs Future","doi-asserted-by":"publisher","first-page":"49","DOI":"10.1358\/dof.1993.018.01.198548","article-title":"Dexmedetomidine, a novel \u03b12-adrenergic agonist. 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