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      Extracellular Amino Acids as Markers of Myocardial Ischemia during Cardioplegic Heart Arrest


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          Extracellular levels of amino acids in the myocardial interstitium are sensitive indicators of myocyte function. Lowered ATP leads to a rapid extracellular appearance of amino acids with a high intra- to extracellular concentration ratio, such as taurine and glutamate. Nitrogen fluxes are reflected by glutamine, while alanine, glycine, serine and leucine are markers of proteolysis. In addition, degradation of membrane phospholipids is reflected by other primary amines, such as phosphoethanolamine. The time course of these changes was determined before, during and after cardioplegic heart arrest. Two regions of the heart were monitored in 20 patients by means of microdialysis sampling. After only 20 min of heart arrest, extracellular taurine, glutamate and phosphoethanolamine increased transiently up to 25 times the basal level. Ten–20 min later, glutamine increased by 6 times. A doubling of alanine, glycine, serine and leucine levels took place 30 min after release of the aortic cross-clamp. After 2 h, all were at levels similar to those recorded 15–30 h later. Levels of taurine and glutamate in the anterior wall of the heart correlated significantly with those of its lateral wall. The response to surgery and heart arrest was studied in a group of patients with ischemic heart disease as well as in another group of patients, who underwent heart surgery for nonischemic reasons. The response of taurine and glutamine was significantly higher for the patients with ischemic heart disease, in spite of a shorter mean time of heart arrest. No sex differences were recorded. High levels of amino acids coincided frequently with clinical events, which were suggestive of ischemia, but were also recorded in a few patients without diagnosed events. We conclude that monitoring of extracellular amino acids is valuable for evaluation and development of cardioprotective strategies.

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          Lipid Peroxidation and Cardiac Troponin T Release during Routine Cardiac Surgery

          Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation. The purpose of this study was to monitor perioperative changes of cardiac troponin t and malondialdehyde as an indicator of lipid peroxidation in patients who underwent routine cardiac operation and had no signs of perioperative myocardial infarction. Patients with thoracic surgery alone served as controls. We studied 20 patients with cardiopulmonary bypass (CPB) and 9 patients with other thoracic operations. Serum troponin t, malondialdehyde, myoglobin, creatine kinase (CK) including CK-MB isoenzyme levels were monitored before CPB, immediately after cessation of CPB, 20 and 44 h after CPB. Patients with signs of myocardial infarction before or up to 44 h after surgery were excluded. Of 20 patients with CBP, 18 patients showed a significant increase of troponin t and 16 patients had elevated malondialdehyde serum levels following CPB. Troponin t serum values were raised immediately after CPB to 0.60 ± 0.12 µg/l and increased further to 0.90 ± 0.17 µg/l after 44 h (p < 0.005, in comparison to preoperative: 0.08 ± 0.02 µg/l). Patients undergoing the other thoracic operations showed neither any detectable troponin t serum values nor significant changes of serum malondialdehyde during the observed period. In the CPB group serum malondialdehyde peaked immediately after CPB to 98 ± 9 nmol/g albumin (p < 0.005) and returned to preoperative levels (63 ± 3 nmol/g albumin) within 20 h (60 ± 3 nmol/g albumin). Individual maximal troponin t serum levels did not correlate with individual maximal serum malondialdehyde levels. The observed increase of troponin t levels had no influence on patients’ outcome followed up for 18 months. The results demonstrate that troponin t and lipid peroxidation increase during uncomplicated cardiac surgery in patients without signs of myocardial infarction. Following uncomplicated cardiac surgery, a moderate increase of cardiac troponin t may not reflect severe cardiac injury.

            Author and article information

            S. Karger AG
            June 1999
            18 June 1999
            : 91
            : 1
            : 31-40
            Departments of aThoracic and Cardiovascular Surgery, bInternal Medicine, and dAnatomy and Cell Biology, University of Göteborg, Sweden; cDepartment of Heart Surgery, University of Insubria, Varese, Italy
            6874 Cardiology 1999;91:31–40
            © 1999 S. Karger AG, Basel

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            Page count
            Figures: 3, Tables: 4, References: 38, Pages: 10
            Cardiac Surgery

            General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
            Taurine,Amino acids,Glutamine,Myocardium,Ischemia,Glutamate,Microdialysis


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