Cardioplegic solutions and nitric oxide in coronary artery bypass surgery/Koroner arter baypas cerrahisinde nitrik oksit ve kardiyoplejik solusyonlari.

In the study by Karaca et al. (1), published in the current issue of the journal authors have shown that use of blood cardioplegia in the reperfusion period after aortic cross clamp in patients with diabetes mellitus type II undergoing coronary artery bypass grafting surgery was superior to crystalloid solution in terms of myocardial protection as assessed by the degree of nitric oxide (NO) release.

Vascular tone is regulated by vasodilators and vasoconstrictors. Nitric oxide is the primary vasodilator peptide that causes relaxation of vascular smooth muscle, whereas endothelin-1 (ET-1) is the predominant vasoconstrictor peptide that constricts vascular smooth muscle (2).

During coronary artery bypass grafting, the heart is arrested and subjected to ischemia-reperfusion injury. The injury may involve coronary endothelium and NO mechanisms. Many studies have shown that an important feature of ischemia-reperfusion injury is the post-ischemic endothelial dysfunction, which impairs NO release (3, 4). It has been experimentally and clinically shown that this harmful effect can be alleviated by Larginine administration, which is a nitric oxide precursor (5, 6). However, some studies have shown that the release of NO increases after tepid or normothermic cardiopulmonary bypass showing that NO release is affected by the temperature used (7). Hypothermia decreases NO release whereas tepid or normothermic cardioplegia increases NO release. In this study (1), although the cardiopulmonary bypass temperature was constant, the crystalloid cardioplegia temperature was usually at +4 [degrees]C. Because the blood cardioplegia prepared in the other group was warmer than this temperature, this might be the factor affecting differences of NO release between the two groups.

In diabetic patients the endothelial function and mediator release, which affect this function (NO and ET) are different from non-diabetics (8). Sharma et al. (9) found that diabetic patients appear to differ significantly from the non-diabetic population in that there is a significant increase in coronary affluent ET-1 during reperfusion periods after coronary artery bypass grafting without concomitant increases in NO concentrations. On the other hand, Donatelli et al. (10) did not find any difference in ET-1 concentrations between diabetic and non-diabetic patients with coronary artery disease.

Despite developments in surgery, anesthesia, and myocardial protection Type II diabetes, requiring treatment with insulin or oral antidiabetic drugs, is associated with an increased early and long-term risk of death or acute myocardial infarction after coronary artery bypass grafting (11). It is important that this study showed blood cardioplegia protects endothelial functions better than crystalloid cardioplegia through protection of NO release.

References

(1.) Karaca P, Yurtseven N, Enc Y , Aksoy T, Sokullu O, Bilgen F, et al. Effects of different cardioplegic solutions on no release from coronary vasculature in diabetic patients undergoing coronary artery bypass surgery. Anadolu Kardiyol Derg 2006: 6; 347-51.

(2.) Vane JR, Anggard EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990; 323: 27-36.

(3.) Gohra H, Fujimura Y, Hamano K, Noda H, Katoh T, Zempo N, et al. Nitric oxide release from coronary vasculature before, during, and following cardioplegic arrest. World J Surg 1999; 23: 1249-53.

(4.) Amrini M, Chester AH, Jayakumar J, Schyns CJ, Yacoub MH. Larginine reverses low coronary reflow and enhances postischemic recovery of cardiac mechanical function. Cardiovasc Res 1995; 30: 200-4.

(5.) Hatsuoka S, Sakamoto T, Stock UA, Nagashima M, Mayer JE Jr. Effect of L-arginine or nitroglycerine during deep hypothermic circulatory arrest in neonatal lambs. Ann Thorac Surg 2003; 75: 197-203.

(6.) Amrani M, Gray CC, Smolenski RT, Goodwin AT, London A, Yacoub MH. The effect of L-arginine on myocardial recovery after cardioplegic arrest and ischemia under moderate and deep hypothermia. Circulation 1997; 96(9 Suppl): 197-203.

(7.) Ohata T, Sawa Y, Kadoba K, Kagisaki K, Suziki K, Matsuda H. Role of nitric oxide in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass. Eur J Cardio-Thorac Surg 2000; 18:342-7.

(8.) De Meyer GR, Herman AG. Vascular endothelial dysfunction. Prog Cardiovasc Dis 1997; 39: 325-42.

(9.) Sharma AC, Fogelson BG, Nawas SI, Vigneswaran WT, Sam AD 2nd, Alden KJ, et al. Elevated coronary endothelin-1 but not nitric oxide in diabetics during CABG. Ann Thorac Surg 1999; 67: 1659-63.

(10.) Donatelli M, Hoffmann E, Colletti I, Andolina G, Russo V, Bucalo ML, et al., Circulating endothelin-1 levels in type 2 diabetic patients with ischaemic heart disease. Acta Diabetol 1996; 33: 246-8.

(11.) Alserius T, Hammar N, Nordqvist T, Ivert T. Risk of death or acute myocardial infarction 10 years after coronary artery bypass surgery in relation to type of diabetes. Am Heart J 2006; 152: 599-605.

Riza Turkoz Department of Cardiovascular Surgery, Medical Faculty, Baskent University Adana Training and Research Hospital, Adana, Turkey

Address for Correspondence: Dr. Riza Turkoz, Baskent Universitesi Tip Fakultesi, Kalp Damar Cerrahisi Anabilim Dali, Adana Uygulama ve Arastirma Hastanesi, Dadaloglu mah., 39 sok. no:6 01250 Yuregir, Adana, Turkiye Tel.: [phone]/1204 Fax: [phone] E-mail: [e-mail]