The anatomy features and surgical significance of the pulmonary circuits of pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries / 中华外科杂志

<p><b>OBJECTIVES</b>To analyze the anatomy features of the pulmonary circuits in the patients with pulmonary atresia (PA) with ventricular septal defect (VSD) and major aortopulmonary collateral arteries (MAPCA), and discuss the clinical significance.</p><p><b>METHODS</b>From April 2002 to June 2010, the anatomy features of pulmonary circuits in 33 patients with PA/VSD/MAPCA were examined and analyzed. There were 21 male and 12 female patients. The age ranged from 11 months to 29 years. The anatomic types of PA/VSD included group B for 22 cases, group C for 11 cases. Thirty-one patients of them underwent 33 operative procedures. The operations included aorta-pulmonary shunt in 8 cases, one stage unifocalization with VSD open in 2 cases, complete repair in 23 cases.</p><p><b>RESULTS</b>Twenty-nine (87.9%) patients had native pulmonary arteries, 6 of them were normal size and 23 were hypoplastic size. Four patients (12.1%) had no native pulmonary arteries. The postoperative oxygen saturation of the patients undergone shunt and one stage unifocalization was increased to 83% to 90%. There was one early death after complete repair because of multiorgan function failure. There were 4 cases of severe low cardiac output and 3 cases of respiratory function failure. Sixteen patients after complete repair were followed up more than one year. The postoperative right ventricular pressure was 41 to 99 mmHg (1 mmHg = 0.133 kPa). The ejection fraction value was more than 50% in 14 patients and less than 50% in 2 patients. Two patients had medium pulmonary insufficiency.</p><p><b>CONCLUSIONS</b>An individualized approach based on the anatomy of the pulmonary circuits permits achievement in the patients with PA/VSD/MAPCA. The surgical strategy for PA/VSD/MAPCA mainly depends on the anatomy features of native pulmonary arteries, confluent pulmonary arteries and MAPCA.</p>

Role of nitric oxide during early phase myocardial ischemic preconditioning in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>To date, there have been no reports on altered nitric oxide (NO) content in ischemia/reperfusion with regard to in vivo preconditioning procedures. These studies are important for understanding the mechanisms of NO during early myocardial ischemic preconditioning. The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate (cGMP), as well as activity of nitric oxide synthase (NOS) in ischemia/reperfusion with respect to preconditioning in rats.</p><p><b>METHODS</b>Sixty-six female Sprague-Dawley rats were randomly divided into four groups: ischemic preconditioning group (IP), ischemia/reperfusion group (I/R), control group (CON), and preconditioning procedure group (PC). In the PC group, rats were further divided into PC1-, PC1 +, PC2-, PC2 +, PC3-, and PC3 + subgroups. Rats underwent left coronary artery occlusion and reperfusion, and subsequently, NOS activity and levels were assessed with spectrophotometric analysis. cGMP contents were measured with radioimmunoassay.</p><p><b>RESULTS</b>The level of NO and cGMP, as well as the activity of NOS, were significantly higher in the IP group compared to the I/R and CON groups (P < 0.05). During preconditioning prior to prolonged ischemia, NO and cGMP levels varied markedly with ischemia and reperfusion. The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute ischemia, and were almost completely reversed during each reperfusion period. NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning.</p><p><b>CONCLUSIONS</b>NO plays an important role during early phase myocardial ischemic preconditioning in rats. NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning. Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected. NO and cGMP fluctuations might be the trigger for protection during early phase myocardial ischemic preconditioning.</p>

Clinical analysis of surgical procedures and outcomes for corrected transposition of great arteries with heart anomaly / 中华外科杂志

<p><b>OBJECTIVE</b>To determine the outcome of anatomically corrective repair and traditional repair of corrected transposition of great arteries (c-TGA) with heart anomaly.</p><p><b>METHODS</b>From April 2002 to December 2006, nineteen patients including fourteen male and five female with c-TGA, underwent operations, age ranged from 2 to 22 years old and weight ranged from 10 to 48 kg. Fifteen of them received anatomically corrective repair and the other four received traditional repair. Eighteen patients were referred to SLL (segmental anatomy) in situs solitus while fifteen of them with levocardia and three with dextrocardia. One patient was referred to IDD (segmental anatomy) in situs inversus with levocardia. Associated cardiac lesions included ventricular defect in eighteen patients, double outlet of right ventricle in one patient, pulmonary stenosis in seventeen patients and pulmonary hypertension in two patients. The operative procedures to anatomically correct atrioventricular discordance included an atrial switch plus a ventricle-arterial switch. The atrial switch was performed using the modified Senning procedure (n=13), Senning procedure (n=1) and Mustard procedure (n=1). The ventricle-arterial switch was performed using a Rastelli procedure (n=13) or an arterial switch (n=2). The patients underwent Mustard and Rastelli procedure had received bi-direct Gleen shunt due to postoperative high pressure of superior vena cava. Three patients underwent traditional cardiac repair because of small ventricular septal defect and one patient was reoperated to undergo traditional cardiac repair because of left ventricular failure after received anatomically corrective repair.</p><p><b>RESULTS</b>In the patients received anatomically corrective repair, there was one early operative death received a modified Senning atrial switch and an arterial switch. The cause of death was acute myocardial failure due to imperfect coronary transfer. The postoperative complications included severe low cardiac output syndrome (n=1), temporary atrioventricular block (n=1) and thorax cavity fluidify (n=1). The survivors were followed up for 6 months to 4 years. All were sinus cardiac rhythm and in NYHA class I or II. There was no death in the patients received traditional repair. Four patients were followed up for 1 year. Three patients were in NYHA I or II class and one patient in class II.</p><p><b>CONCLUSIONS</b>Anatomically corrective repair of c-TGA can be performed with good operative survival and intermediate-term outcome. The patients with good right ventricular function and well developed tricuspid valve who were difficult to undergo anatomically corrective repair might be fit to receive traditional repair.</p>

Study of cardiopulmonary adaptation during exercise in patients after extracardiac conduit total cavopulmonary connection / 中华外科杂志

<p><b>OBJECTIVE</b>To study cardiopulmonary physiology during exercise in patients after extracardiac total cavopulmonary connection (ECTCPC).</p><p><b>METHODS</b>Twenty-six patients were studied after ECTCPC by exercise testing with bicycle treadmill protocol. Heart rate (HR), blood pressure (BP), respiratory frequency (RF) and pulse oxygen saturation (SpO(2)) were measured continuously; twenty-six patients suffered from Fallot 4 underwent biventricular repair were also studied as control group.</p><p><b>RESULTS</b>In ECTCPC group, HR, BP, SpO(2) and RF all increased with exercise below 3 grade; when exceed 4 grade, BP, SpO(2) decreased and RF kept increasing. Compared with control group, HR, RF were higher (t = 2.13, P < 0.05; t = 2.31, P < 0.05), SpO(2) was lower (t = 2.46, P < 0.05) under the quiescent condition; When exceed 3 grade, HR, BP, SpO(2) decreased more significantly, but RF increased continuously. In fenestration group after ECTCPC, HR reached the top at 5 grades, but in group without fenestration it reached the top at 3 grades; In the whole process of exercising, RF kept higher and SpO(2) kept lower in fenestration group.</p><p><b>CONCLUSIONS</b>The ECTCPC patients showed obviously exercise limitation. Totally bypass of sinoatrial node in this operation may have some adverse effects on the integer regulation of HR.</p>

The effects of inhaled nitric oxide on pulmonary vascular resistance in patients after total cavopulmonary connection / 中华外科杂志

<p><b>OBJECTIVE</b>To study the effects of inhaled nitric oxide (NO) on pulmonary vascular resistance in patients after total cavopulmonary connection (TCPC).</p><p><b>METHODS</b>Fifty-two patients after TCPC were evaluated, of them 24 patients were administered with inhaled nitric oxide in the early postoperative period. The cardiac index (CI) and pulmonary vascular resistance (PVR) were compared before and after inhaled NO.</p><p><b>RESULTS</b>In experimental group, after inhaled NO, partial pressure of oxygen in artery/fraction of inspired oxygen increased from 161 +/- 17 to 193 +/- 23 (t = 2.75, P < 0.01); CI from (2.86 +/- 0.24) L.min(-1).m(-2) to (3.13 +/- 0.22) L.min(-1).m(-2) (t = 2.25, P < 0.05); PVR decreased from (4.2 +/- 0.5) U/m(2) to (3.8 +/- 1.4) U/m(2) (t = 2.29, P < 0.05); central venous pressure (CVP) from (17.0 +/- 1.8) mm Hg to (15.0 +/- 1.1) mm Hg, decreased 11.7%. Compared with the control group, respirator time decreased from (86 +/- 27) h to (54 +/- 18) h (t = 2.29, P < 0.05); ICU time from (6 +/- 2) d to (4 +/- 2) d (t = 2.32, P < 0.05); But hydrothorax drainage and length of stay had no significant difference.</p><p><b>CONCLUSIONS</b>Though inhaled NO, there is no significant long-term effects in patients after TCPC, but it may play an important role in the management of low cardiac output syndrome and high cava pressure caused by reactive elevated pulmonary vascular resistance in the early postoperative period of TCPC.</p>