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Research Article Free access | 10.1172/JCI107676
Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway
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Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway
Find articles by Kjekshus, J. in: JCI | PubMed | Google Scholar
Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway
Find articles by Lekven, J. in: JCI | PubMed | Google Scholar
Published May 1, 1974 - More info
Increased delivery of free fatty acids raises myocardial oxygen consumption (ṀVO2) without influencing mechanical performance. The effects of norepinephrine on ṀVO2 and on the size of ischemic injury after acute coronary occlusion were therefore studied before and during inhibition of lipolysis with β-pyridylcarbinol. In spite of similar mechanical responses to norepinephrine, ṀVO2 increased by 57±11% before and significantly less, 31±6%, (P < 0.01) during inhibition of lipolysis. After coronary occlusion the ischemic injury associated with norepinephrine infusion, as evidenced by epicardial mapping of S-T segment elevation, was larger before (7.9±1.1 mV) than during inhibited lipolysis (2.8±0.4 mV; P < 0.005). Average S-T segment elevation associated with norepinephrine infusion during inhibited lipolysis (2.8±0.4 mV) was even lower (P < 0.05) than during control occlusion alone, before drug administration (4.4±0.7 mV). In conjunction with an antilipolytic agent, norepinephrine was shown to reduce the extent and magnitude of the myocardial ischemic injury produced by acute coronary occlusion; this could be due to an improved balance between myocardial oxygen supply and requirement.
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