Changes of plasma asymmetric dimethylarginine levels after coronary artery bypass grafting

• Published in: Scandinavian cardiovascular journal : SCJ Vol. 40; no. 6; pp. 363 - 367
• Main Authors: Karu, Inga, Zilmer, Kersti, Starkopf, Joel, Zilmer, Mihkel
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.12.2006; Taylor & Francis
• Subjects: ADMA; Arginine - analogs & derivatives; Arginine - blood; Arginine - metabolism; Asymmetric dimethylarginine; Cardiopulmonary Bypass; coronary artery bypass; Coronary Artery Bypass - methods; Coronary Disease - blood; Coronary Disease - metabolism; Coronary Disease - surgery; Female; Heart Arrest, Induced; Humans; hyperoxia; Hyperoxia - blood; Male; Middle Aged; Myocardium - metabolism; Postoperative Period; preconditioning; Time Factors
• ISSN: 1401-7431; 1651-2006
• DOI: 10.1080/14017430600983648

Objectives. We investigated whether coronary artery bypass grafting affects plasma asymmetric dimethylarginine (ADMA) concentrations and whether precardioplegic hyperoxia influences ADMA release from the heart. Design. Twenty two patients were randomized into control (n = 11) and hyperoxia (n = 11, ventilated with >96% oxygen before cardiopulmonary bypass) groups. Arterial and coronary sinus blood was sampled before cardioplegia and during early reperfusion. Arterial samples were drawn 60 min after declamping of the aorta, and on the first postoperative day. Results. Baseline arterial values of ADMA were not different between groups (0.59±0.18 µmol/l control, 0.63±0.13 µmol/l hyperoxia group). Negligible release of ADMA into coronary sinus was detected 20 min after cardioplegia. A significant decrease of arterial ADMA was observed by the first postoperative morning (0.42±0.16 µmol/l in control, and 0.38±0.07 in hyperoxia group, p < 0.01 compared to baseline). Conclusions. CABG with cardioplegia is associated with decrease of ADMA by the first postoperative morning. Reperfusion of cardioplegic heart did not result in significant release of ADMA. Pretreatment with hyperoxia had no influence on myocardial release and arterial levels of ADMA.