[show abstract][hide abstract] ABSTRACT: We investigated the myocardial protective effect of a moderate-potassium cold blood cardioplegic solution (K(+), 10 mmol/L) in pediatric cardiac surgery.
Sixty-eight pediatric patients with congenital heart disease and undergoing open heart surgery with cardiopulmonary bypass were randomly allocated to the high potassium (HP [K(+), 20 mmol/L, n = 31]) cold blood cardioplegia group or the moderate potassium (MP [K(+), 10 mmol/L, n = 37]) cold blood cardioplegia group. Heart arresting time, rhythm recovery time, mechanical ventilation time, inotropic drug use in the intensive care unit, perioperative serum cardiac troponin I concentrations, morbidities, and mortalities were compared between the two groups.
There were no differences in cardiopulmonary bypass time, aorta cross-clamping time, cardioplegia volume, lowest body temperature during cardiopulmonary bypass, total volume of cardioplegia delivered, hematocrit value, and fluid output during the operation between the two groups. However, there was a longer arresting time and a shorter rhythm recovery time in the MP group (35.6 ± 2.4 s, and 30.8 ± 3.1 s) when compared with that in the HP group (24.7 ± 2.7 s, and 42.0 ± 4.0 s, both p < 0.05). The total mediastinal drainage volume, the length of stay in the intensive care unit, the postoperative inotropic drug use, and the postoperative hospital time were similar between the two groups, but the number of patients with a long postoperative mechanical ventilation time (>24 hours) in the MP group (6 of 36) was less than that in HP group (13 of 30; p < 0.05). At 1 hour, 3 hours, and 6 hours after myocardium reperfusion, the serum concentration of cardiac troponin I significantly decreased in the MP group (in ng/mL: 15.18 ± 3.57, 24.83 ± 4.91, and 19.62 ± 3.93, respectively) when compared with that in the HP group (in ng/mL: 32.67 ± 5.31, 39.26 ± 7.43, and 30.52 ± 5.17, respectively, p < 0.05).
The present study demonstrated that the M (10 mmol/L) cold blood cardioplegia formula is associated with better myocardial protective effects when compared with conventional HP cardioplegia in pediatric patients.
The Annals of thoracic surgery 07/2012; 94(4):1295-301. · 3.74 Impact Factor
[show abstract][hide abstract] ABSTRACT: The calcium paradox represents an important model in which to study myocardial injuries due to intracellular Ca(2+) overload. In a previous study, calpain was transiently activated in Ca(2+) -paradoxic hearts. The aim of the present study was to determine the role of calpain in myocardial dysfunction in hearts subjected to the Ca(2+) paradox and to elucidate the underlying mechanisms. Rat hearts were isolated, Langendorff perfused and subjected to the Ca(2+) paradox, which was induced by 3 min Ca(2+) depletion followed by 30 min Ca(2+) repletion, in the presence or absence of the calpain inhibitor 10 umol/L MDL 28170. Cardiac function was evaluated. Furthermore, cell death and the degradation of troponin I (TnI) were assessed and calpain activity was determined by measurement of the α-fodrin fragment and confocal image analysis. Upon Ca(2+) repletion, the hearts immediately deteriorated, exhibiting a marked depression in cardiac function and an enlarged myocardial injury area. This was accompanied by significant increases in lactate dehydrogenase, mitochondrial release of cytochrome c, the apoptotic index and degraded TnI. These changes were significantly inhibited by MDL 28170, with the exception of TnI degradation. Compared with the control group, Ca(2+) -paradoxic hearts showed a marked increase in cleaved 150 kDa fragments resulting from specific calpain-mediated proteolysis of α-fodrin. This effect was attenuated by MDL 28170. Confocal image analysis revealed the translocation of both μ- and m-calpain to the sarcolemmal membrane in Ca(2+) -paradoxic hearts, indicating increased activity of both isoforms. The results suggest that the Ca(2+) paradox promotes calpain activity, leading to necrosis, apoptosis and myocardial dysfunction.
Clinical and Experimental Pharmacology and Physiology 02/2012; 39(4):385-92. · 2.16 Impact Factor
[show abstract][hide abstract] ABSTRACT: We sought to evaluate a moderate-potassium cardioplegic solution using adenosine and lidocaine as the arresting and protecting cardioprotective combination in pediatric cardiac surgery.
One hundred thirty-four patients with congenital heart disease were randomly allocated to one of 3 groups according to the cardioplegia formula used: the high-potassium (HP) group (K(+), 20 mmol/L), 46 patients; the high-potassium adenosine-lidocaine (HPAL) group (K(+), 20 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients; and the moderate-potassium adenosine-lidocaine (MPAL) group (K(+), 10 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients. Hemodynamic data during the operation and postoperative data were recorded. Serum cardiac troponin I concentrations were examined at the time points of before cardiopulmonary bypass and 1, 3, 6, 12, and 24 hours after aortic crossclamp removal.
At the end of cardiopulmonary bypass and modified ultrafiltration, the systolic and pulse pressures of the MPAL group were significantly increased compared with the respective values of the HP group. At the time points of 1 to 12 hours after reperfusion, the levels of serum cardiac troponin I were significantly decreased in the MPAL group compared with those in the HP and HPAL groups.
The MPAL cardioplegia formula was associated with better myocardial protective effects.
The Journal of thoracic and cardiovascular surgery 01/2009; 136(6):1450-5. · 3.41 Impact Factor