L-arginine effects on myocardial stress in cardiac surgery: preliminary results.
BACKGROUND
L-arginine in addition to cardioplegia stimulates the release of nitric oxide and increases coronary blood flow, decreasing platelet activation and leukocyte adhesion. The aim of our study was to determine the feasibility and the efficacy of the addition of L-arginine to antegrade and retrograde blood cardioplegia in reducing myocardial damage and stress.


METHODS
Twenty-eight consecutive patients who underwent coronary artery bypass grafting were randomized to receive 7.5 g of L-arginine in 500 ml of cardioplegic solution. To assess safety of use of L-arginine, hemodynamic evaluation was performed before sternum opening, at sternum closure, and 1 hour after arrival in the intensive care unit to measure cardiac index, systemic and pulmonary vascular resistances, and pulmonary capillary wedge pressure. Moreover, transesophageal echocardiography was performed to assess myocardial contractility. To determine the effects on myocardial stress, blood samples were taken from the retrograde coronary sinus catheter for lactate, interleukin (IL)-2 receptor, IL-6 and tumor necrosis factor (TNF)-alpha levels. Serum samples (preoperatively, 2, 18 and 42 hours after aortic cross-clamping removal) were also analyzed to measure creatine phosphokinase, creatine kinase-MB mass, cardiac troponin T, platelets, and leukocytes.


RESULTS
We found statistical differences for IL-2 receptor, IL-6, TNF-alpha, platelets and leukocytes, in favor of the treated group, and decreasing trends in creatine kinase-MB mass and troponin T levels.


CONCLUSIONS
The present study shows the positive effects of the addition of L-arginine to cardioplegia. Reduced IL-2 receptor, IL-6 and TNF-alpha indicate a decrease in myocardial stress. Safety of Larginine is related to lower values of systemic vascular resistances and pulmonary capillary wedge pressure observed in group A postoperatively that could improve the patient's outcome in terms of a reduced need for inotropic support. Moreover, the decrease in platelet and leukocyte count in the treated group might express a reduced no-reflow phenomenon and a better reperfusion, limiting endothelial injury from oxygen radical production.
Colagrande
Luisa
L
Surgical Science and Intensive Care Department, Cardiac Surgery Clinic, University of Milan-Bicocca, San Gerardo Hospital, Monza, Italy. lcolagrande@yahoo.it
Formica
Francesco
F
Porta
Fabiano
F
Brustia
Matteo
M
Avalli
Lionello
L
Sangalli
Fabio
F
Muratore
Maria
M
Paolini
Giovanni
G
D001120:Arginine / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001026:Coronary Artery Bypass / Q000009:adverse effects / Q000379:methods*; D052279:Creatine Kinase, MB Form / Q000097:blood; D017548:Echocardiography, Transesophageal; D005500:Follow-Up Studies; D006324:Heart Arrest, Induced / Q000009:adverse effects; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D007432:Intraoperative Period; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000601:surgery*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D015375:Receptors, Interleukin-2 / Q000097:blood; D012189:Retrospective Studies; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology
D015415:Biomarkers; D015850:Interleukin-6; D015375:Receptors, Interleukin-2; D020107:Troponin T; D014409:Tumor Necrosis Factor-alpha; D001120:Arginine; D052279:Creatine Kinase, MB Form