ABSTRACT
<p><b>BACKGROUND</b>Current knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide (H2S) has been identified as a novel endogenous vasodilator and neuromodulator due to its antioxidation capacity. However, whether H2S pretreatment in neonatal mouse cardiomyocytes is a protection effect against oxidative stress remains elusive.</p><p><b>METHODS</b>Primary neonatal mouse cardiomyocytes were isolated and cultured, subsequently, pretreated with the H2S donor, sodium hydrosulfide (NaHS). Cell viability, lactate dehydrogenase (LDH) release, and reactive oxygen species (ROS) production are evaluated. The levels of superoxide dismutase (Sod2) and Sirtuin 1 (Sirt1), a deacetylation enzyme, were detected by Western blotting. The statistics was performed using independent-sample t-test.</p><p><b>RESULTS</b>NaHS (100 μmol/L) had no toxicity to primary neonatal mouse cardiomyocytes. Furthermore, NaHS pretreatment significantly improved neonatal mouse cardiomyocytes survival after H2O2-induced cell death, indicated by the decrease in LDH release (40.00 ± 2.65% vs. 65.33 ± 4.33%, P < 0.01) and ROS production (1.90 ± 0.33 vs. 4.56 ± 0.56, P < 0.05), and that the salubrious effect was accompanied by the upregulation of Sod2 expression. In addition, the study showed that NaHS pretreatment improved mitochondrial DNA number in neonatal mouse cardiomyocyte. Furthermore, the result demonstrated NaHS increased the expression of Sirt1 in neonatal mouse cardiomyocyte. Ex 527, an inhibitor of Sirt1, could attenuate these effects of NaHS-induced Sod2 expression and mtDNA number increase, furthermore, abrogate the cytoprotective effects of NaHS for neonatal mouse cardiomyocytes.</p><p><b>CONCLUSION</b>Sirt1 mediated H2S-induced cytoprotection effects in neonatal mouse cardiomyocytes.</p>
ABSTRACT
<p><b>BACKGROUND</b>Congenital heart defects with intractable hypoplasia of the pulmonary arteries without intercourse or with intercourse stenosis is unsuitable for surgical correction or regular palliative procedures. We reported our experience with combined palliative procedures for congenital heart defects with intractable hypoplasia pulmonary arteries.</p><p><b>METHODS</b>From 2001 to 2012, a total of 41 patients with cyanotic congenital heart defects and intractable hypoplasia of the pulmonary arteries underwent surgical procedures. From among them, 31 patients had pulmonary atresia with ventricular septal defect (VSD) and the other 10 cases had complicated congenital heart defects with pulmonary stenosis. Different kinds of palliative procedures were performed according to the morphology of the right and left pulmonary arteries in every patient. If the pulmonary artery was well developed, a Glenn procedure was performed. A modified Blalock-Taussig shunt or modified Waterston shunt was performed if pulmonary arteries were hypoplastic. If the pulmonary arteries were severely hypoplastic, a Melbourne shunt was performed. Systemic pulmonary artery shunts were performed bilaterally in 25 cases. A systemic-pulmonary shunt was performed on one side and a Glenn procedure was performed contralaterally in 16 cases. Major aortopulmonary collateral arteries were unifocalized in six cases, ligated in two cases and interventionally embolized in two cases. There was one early death because of cardiac arrest and the hospital mortality was 2.4%.</p><p><b>RESULTS</b>Five patients suffered from postoperative low cardiac output syndrome, three had perfusion of the lungs, and two pulmonary infections. Systemic pulmonary shunts were repeated after the original operation in three cases due to the occlusion of conduits. The mean follow-up time was 25 months. The pre- and the post-operation left pulmonary indices were (8.13 ± 3.68) vs. (14.9 ± 6.21) mm(2)/m(2). The pre- and post-operation right pulmonary indices were (12.7 ± 8.13) vs. (17.7 ± 7.78) mm(2)/m(2). The pre- and post-operational pulmonary indices were (20.87 ± 9.43) vs. (32.6 ± 11.7) mm(2)/m(2). They were all significantly increased (P < 0.001). The diameter of the pulmonary artery increased after the modified Blalock-Taussig shunt ((5.51 ± 0.94) mm(2)/m(2) pre-operation vs. (7.01 ± 1.97) mm(2)/m(2) post-operation), the modified Waterston shunt ((5.70 ± 3.96) mm(2)/m(2) pre-operation vs. (9.17 ± 3.62) mm(2)/m(2) post-operation) and the Melbourne shunt ((2.17 ± 0.41) mm(2)/m(2) pre-operation vs. (7.35 ± 2.49) mm(2)/m(2) post-operation) (all P < 0.05). Bilateral pulmonary arteries developed well as compared to their pre-operation development. Hemoglobin decreased from (194 ± 27) to (174 ± 24) g/L (P < 0.05) and peripheral oxygen saturation increased from (65 ± 11)% to (84 ± 6)% (P < 0.001). During the follow-up of 27 to 49 months, ultimate complete repair was performed in four cases and one patient underwent a Glenn procedure.</p><p><b>CONCLUSIONS</b>The procedures should be considered on a case to case basis in patients having hypoplasia of the pulmonary arteries with cyanotic congenital heart defects. Combined palliative operations could be an adequate strategic treatment.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Infant , Male , Follow-Up Studies , Heart Defects, Congenital , General Surgery , Lung Diseases , Palliative Care , Pulmonary ArteryABSTRACT
<p><b>BACKGROUND</b>The best age for the arterial switch operation (ASO) in complete transposition of great arteries with ventricular septal defect is usually considered to be within six months. This is because of severe pulmonary arterial hypertension and pulmonary arterial obstructive pathological changes. There are few reports on ASO surgery in children older than three years old.</p><p><b>METHODS</b>We studied 41 children, including 24 males and 17 females, from January 2010 to December 2011. They were divided into three groups by operation age; 15 patients were < 1 year old, 13 were 1 - 3 years old, and 13 were > 3 years old. Associated cardiac abnormalities included patent ductus arteriosus in six cases, atrial septal defect in five cases, and mitral regurgitation in two cases. All the patients had echocardiography before the operation. Seventeen patients underwent a coronary computed tomography examination and five patients underwent right heart catheterization. All ASO surgeries were performed under inhalation anesthesia and hypothermic cardiopulmonary bypass.</p><p><b>RESULTS</b>Three operative deaths occurred. Two were in the < 1 year old group, who died from severe postoperative low cardiac output. The other was two years old and died of postoperative multiple organ failure. There was no significant difference in postoperative mortality and the recent mid-term survival rate among the three groups. Thirty-eight cases were followed up for an average of 11.2 months, ranging 6 - 20 months. One seven years old patient died of acute diarrhea and electrolyte disturbance arrhythmia caused by food poisoning. Three patients more than three years old still had residual pulmonary arterial hypertension.</p><p><b>CONCLUSION</b>Children older than three years old can still undergo the ASO procedure, but residual pulmonary hypertension is present.</p>