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Ann Thorac Surg 1985;40:20-24
© 1985 The Society of Thoracic Surgeons
Departments of Surgery and Pharmacology, University of Illinois College of Medicine, Chicago, IL
Accepted for publication December 10, 1984.
* Address reprint requests to Dr. Silverman, Department of Surgery, University of Illinois College of Medicine, PO Box 6998, Chicago, IL 60680
Carnitine has therapeutic potential for the postischemic heart by facilitating the oxidation of acylated fatty acid metabolites, the intracellular accumulation of which has a deleterious effect on myocardial function and metabolism. To test this hypothesis, two groups of dogs were given preischemic treatment with carnitine, 50 mg per kilogram of body weight (Group 1) or 100 mg/kg (Group 2), and were compared with untreated controls (N = 12 for all groups). The canine hearts underwent 30 minutes of global 37°C ischemic arrest with reperfusion. Left ventricular systolic and diastolic function was assessed by an intracavitary balloon while metabolic derangements were quantitated by serial myocardial biopsies assayed for adenosine triphosphate (ATP). Comparable 49 to 53% (p < 0.01) declines in preischemic ATP levels occurred during the study period in the controls and both experimental groups. However, postischemic systolic left ventricular function was better preserved in Group 2: these hearts generated 61 ± 3% of preischemic peak developed pressure compared with 37 ± 4% in the controls and 42 ± 3% in Group 1 (p < 0.01 for each), and 60 ± 2% of preischemic maximum rate of rise of left ventricular pressure as opposed to 45 ± 4% in the controls and 49 ± 6% in Group 1 (p < 0.02 for each). Moreover, whereas in the controls, postischemic left ventricular end-diastolic pressure (LVEDP) was progressively 4.7 to 19.4 mm Hg higher than preischemic LVEDP at each 5-ml increase in left ventricular end-diastolic volume (LVEDV) from 5 to 30 ml (p < 0.01 for each increment), the preischemic and postischemic LVEDP versus LVEDV curves of Group 2 were superimposable. Group 1 hearts had the same impaired postischemic compliance as the controls. The data indicate that carnitine has a dissociative and dose-dependent beneficial effect on myocardial ischemia by allowing preservation of ventricular compliance and improved maintenance of contractile function without preventing adenine nucleotide depletion.
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