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The aim of the present study was to examine the post-infarct acute effect of adenosine-5'-triphosphate (ATP) on myocardial infarction (MI) size as well as its precise molecular mechanism. Sixty New Zealand white male rabbits were exposed to 40 min of ischemia followed by 180 min of reperfusion. The rabbits were intravenously administered 3 mg/kg of ATP (ATP group) or saline (control group) immediately after reperfusion and maintained throughout the first 30 min. The wortmannin+ATP, PD-98059+ATP, and 5-hydroxydecanoic acid (5-HD) sodium salt+ATP groups were separately injected with wortmannin (0.6 mg/kg), PD-98059 (0.3 mg/kg), and 5-HD (5 mg/kg) 5 min prior to ATP administration. MI size was calculated as the percentage of the risk area in the left ventricle. Myocardial apoptosis was determined using a TUNEL assay. Western blot analysis was performed to examine the levels of protein kinase B (Akt)/p-Akt and extracellular signal-regulated kinase (ERK)/p-ERK in the ischemic myocardium, 180 min after reperfusion. The infarct size was significantly smaller in the ATP group than in the control group (p

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that hydrolyzes oxidized phospholipids to generate bioactive proatherogenic products. Nonculprit lesions have been assumed to contribute to the pathogenesis of recurrent acute coronary syndrome (ACS). The role of LP-PLA2 in the progression of nonculprit coronary lesions after successful percutaneous coronary intervention (PCI) remains unclear. Our study included 123 patients with ACS who underwent initial PCI and a long-term follow-up (mean interval, one year) with coronary angiography. Among them, 19 patients were diagnosed as the progression of nonculprit lesions, based on the presence of at least one of the following factors: (1) ≥ 10% reduction in the diameter of a preexisting ≥ 50% stenosis; (2) ≥ 30% reduction in the diameter of a < 50% stenosis; and (3) early-onset stenosis with ≥ 30% reduction in the diameter of a segment that was normal on the primary angiogram. Blood sampling was drawn from all patients at 12-14 hours after PCI. The ACS patients with progression had higher total cholesterol (4.47 ± 1.02 mmol/L vs. 3.59 ± 0.57 mmol/L, P < 0.05), higher levels of Lp-PLA2 activity (14.39 ± 6.13 nmol/min/ml vs. 8.86 ± 3.14 nmol/min/ml, P < 0.001) and a higher proportion of multi-vessel disease than those without progression. Multivariate logistic regression analysis showed that Lp-PLA2 activity (β = 0.024, P = 0.005) was an independent predictor for rapid progression of nonculprit coronary lesions. In conclusion, elevated Lp-PLA2 activity is associated with rapid progression of nonculprit coronary lesions in ACS patients who underwent PCI.

OBJECTIVE To investigate the effects of salvianolic acid B (SA-B) on cardiovascular endothelial cell function and platelet activation during myocardial ischemia-reperfusion in rabbits. METHODS A total of 24 New Zealand white rabbits were randomly divided into sham-operated group, ischemia-reperfusion group (untreated group) and SA-B group. The hearts of rabbits in untreated group and SA-B group underwent half an hour of left anterior descending coronary artery (LADCA) occlusion via ligation technology, which was followed by 4 hours of reperfusion to prepared ischemia-reperfusion injury model in vivo. For sham-operated group, the animals were not subjected to occlusion of LADCA. In SA-B treatment group the rabbits were intravenously administered SA-B immediately after LADCA occlusion, and the other two groups were given normal saline in the same way instead of SA-B. The jugular vein bloods of animals were collected before LADCA ligation, half an hour after ligation and after 1-, 4-hour reperfusion, respectively. The content of plasma nitric oxide (NO) was determined by nitrate reductase process. Radioimmunoassay was applied to detect the endothelin (ET) content in plasma and the count of alpha-granule membrane protein-140 (GMP-140) on platelet surface to identify the activation of the platelet. RESULTS No significant difference was observed before and after sham LADCA occlusion in sham-operated group in the contents of NO and ET in plasma (P>0.05), neither was the count of GMP-140 on platelet surface (P>0.05). The content of NO in plasma detected 0.5 h after LADCA occlusion was significantly decreased in untreated group compared with the sham-operated group at the corresponding time, and they were also much lower than that before LADCA occlusion in the sham-operated group (P

Introduction: Aortopulmonary window (APW), a large aortopulmonary septal defect (APSD), is a serious and rare defect within congenital heart diseases. Case report: In this study, we reported an APW case with severe pulmonary arterial hypertension. This patient was successfully treated by transcatheter closure with a muscular ventricular septal defect (VSD) occluder. Conclusion: We had a successful experience with transcatheter closure of a large APW using a muscular VSD occluder. There was no residual shunt or complications during the 6-month follow-up.

Objective: Adenosine-5'-triphosphate (ATP) has been reported to protect the heart from myocardial ischemia/reperfusion injury when administered at the onset of reperfusion and is as effective as mechanical postconditioning. However, whether the protective effect of postconditioning with ATP is mediated through the same signaling pathways as those of ischemic postconditioning is still unclear. We examined the postinfarct acute effect of ATP on myocardial infarct size and its precise molecular mechanism. Methods: Forty-eight New Zealand white male rabbits were exposed to 40 min of ischemia followed by 180 min of reperfusion. Rabbits were intravenously injected 3mg/kg of ATP (ATP group) or saline (control group) immediately after reperfusion within 30min. The wortmannin+ATP, PD-98059+ATP, and 5-hydroxydecanoic acid sodium salt (5-HD)+ATP groups were respectively injected with wortmannin [a phosphatidyl-inositol 3-kinase (PI3-kinase) inhibitor, 0.6 mg/kg], PD-98059 [an extracellular signal regulated protein kinase (ERK) inhibitor, 0.3 mg/kg], and 5-HD [a mitochondrial ATP-dependent K+ (KATP) channel blocker, 5 mg/kg] 5 min before ATP administration. Myocardial infarct size was calculated as a percentage of the risk area of the left ventricle. Myocardial apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) methods. Western blot analysis was performed to examine the signals such as protein kinase B (Akt) and extracellular signal-regulated protein kinase (ERK) in the ischemic myocardium after 180min of reperfusion. Results: The infarct size was significantly smaller in the ATP group (12.8±1.9%) than in the control group (29.1±2.9%). The infarct size-reducing effect of ATP was completely blocked by wortmannin (26.5±2.7%), PD-98059 (27.9±3.2%), and 5-HD (26.1±4.0%). Compared with control group, ATP group significantly reduced cardiomyocytes apoptosis (apoptotic index: 27.0±5.8% vs 10.3±6.0%, P

A 3-month-old female of 5 kg presented with a 4.23 mm isolated perimembranous ventricular septal defect (pmVSD) which was confirmed by transoesophageal echocardiography (TEE) ( Panel A ). Before that, she had suffered from pneumonia twice. Systolic murmurs of Grade 3 could be heard in the third intercostal space, with intense pulmonary second heart sound. As determined with transthoracic echocardiography (TTE) analysis, the dimensions of the pmVSD were 4.5 mm, with enlarged left atria and ventricles. A 46 mmHg pulmonary artery systolic pressure was estimated by TTE. Cardiomegaly (cardiothoracic ratio: 0.65) and pulmonary congestion were demonstrated on chest X-ray film. All the above features strongly indicated …