Myocardial ischemia-reperfusion injury involves necrosis and apoptosis. The inhibition of angiotensin-converting enzyme (ACE) has been reported to suppress infarct size. In this study, it was investigated whether an ACE inhibitor affected myocardial apoptosis and apoptosis-related proteins in rats with experimental myocardial infarction. Anesthetized Sprague-Dawley rats were divided into four groups. Group I underwent 30 minutes of left coronary artery occlusion followed by 24 hours of reperfusion (control group); Group II underwent oral administration of the ACE inhibitor quinapril (10 mg/kg/day) before coronary occlusion (quinapril group); Group III underwent administration of the bradykinin B(2)-receptor antagonist Hoe 140 (250 microg/kg/day, subcutaneously) with quinapril (quinapril + Hoe 140 group); and Group IV underwent administration of Hoe 140 alone (Hoe 140 group). After reperfusion, myocardial infarct size was determined by triphenyltetrazolium chloride staining. Myocardial apoptosis was detected immunohistologically using terminal deoxynucleotidyl transferase-mediated nick end labeling staining and DNA electrophoresis. Myocardial caspase-3 activation was analyzed by Western blot and the expressions of Bcl-xL and Bax proteins were detected immunohistochemically. Quinapril significantly reduced the ratio of myocardial infarct size in the ischemic area at risk. In addition, quinapril significantly suppressed the incidence of apoptotic myocytes around the necrotic region (from 18.9 +/- 0.8% to 8.6 +/- 1.0%; P < 0.0001), the intensity of DNA ladder formation, and the activation of caspase-3. Hoe 140 attenuated these protective effects of quinapril. In the immunohistochemical study, Bax and Bcl-xL were expressed in myocytes, and ischemia-reperfusion abolished both proteins in the center region of ischemia. The Bax staining was equally observed among all groups. However, Bcl-xL staining remained in the ischemic area widely after quinapril treatment. In addition, Hoe 140 also depleted this effect of quinapril. These results suggest that inhibition of ACE reduces myocardial infarction and apoptosis via the bradykinin B(2) receptor in part. The antiapoptotic effect of the ACE inhibitor is attributed to the changing expression of Bcl-xL.
We assessed several pharmacological effects on electrocardiogram parameters and effective refractory period (ERP) in a patient with a short QT syndrome (SQTS). Pharmacological challenge tests revealed that disopyramide and selective I(kr) blocker, nifekalant normalized QT interval, and ERP of the atrial and ventricular myocardium. This study suggested that disopyramide and nifekalant should be feasible for the drug treatment of the SQTS. Moreover, QT interval was paradoxically prolonged at higher heart rates induced with isoproterenol infusion or an exercise test, although the mechanism of this QT prolongation remains to be investigated.
ulmonary vein varix is a rare abnormality, often presenting as a pulmonary or mediastinal mass on chest roentgenograms, and pulmonary angiography, computed tomography (CT), or magnetic resonance imaging (MRI) is considered necessary for diagnosis. We describe our experience with an unusual case of pulmonary vein varix that was diagnosed noninvasively by echocardiography alone. Case ReportA 47-year-old woman was admitted because of chest discomfort. She did not have a history of cardiovascular disease and the results of physical examination, routine blood tests and electrocardiography were unremarkable. Chest radiography suggested a mediastinal mass inside the left cardiac border in the posteroanterior view ( Fig 1A) and behind the cardiac silhouette in the lateral view (Fig 1B). Two-dimensional transthoracic echocardiography (TTE) was performed. On the parasternal long-axis view, the motion and chamber size of the left ventricle were normal, and there was no enlargement of the left atrial or right ventricular chambers. On the short-axis view and apical 4-chamber view, an echo-free mass was observed outside the posterolateral wall of the left atrium (Fig 2A,B). There was no indentation of the left ventricular wall, suggesting that the mass was an extrapericardial structure. Color Doppler echocardiography detected blood flow from the mass into the left atrium (Fig 2C). Mitral regurgitation was not evident. Transesophageal echocardiography (TEE) more clearly demonstrated dilatation of the pulmonary vein in the proximal left lower lobe with normal intrapulmonary venous connections (Fig 3A,B). The varix communicated with the left atrium. The right pulmonary veins and left upper pulmonary vein were normal. The wall of the varix was Pulmonary vein varix is a rare abnormality, often resembling a pulmonary or mediastinal mass on chest radiographs, and pulmonary angiography has been the mainstay of diagnosis. An unusual case of pulmonary vein varix was clearly defined by echocardiography performed in a 47-year-old woman with chest discomfort who had been found to have an abnormal structure behind the cardiac silhouette on a chest radiograph.
We identified a case of paroxysmal atrial fibrillation (AF) originating from inferior vena cava (IVC) and the low-posterior left atrium (LA). Both foci, the IVC and the low-posterior LA, simultaneously served not only as trigger but also as driver for maintenance of AF. During AF, the IVC and the low-posterior LA continuously demonstrated the rapid and fractionated potentials that exit into both atria with conduction block. Focal ablation for ectopic beats within the IVC and the low-posterior LA completely eliminated the storm of AF.
In nuclear power plants, concretes used for biological shielding walls are exposed to radiation such as neutrons and gamma rays over the long-term operation of the plant. Previous studies have reported that neutron irradiation causes aggregate expansion due to the metamictization of quartz and feldspar leading to reduced density and a loss of the compressive strength and Young's modulus of the concrete. Therefore, it is crucial to understand the current state of a concrete biological shield (CBS) and predict its future soundness. In this study, a rigid-body spring model, which can easily evaluate fracture behavior by using springs between each element, is used to conduct numerical analyses on a CBS. A three-phase (mortar, aggregate, and interfacial transition zone) model of a 2000 mm thick CBS is used to investigate the varying deformation responses depending on the presence or absence of reinforcing bars (rebar), creep, and an inner steel plate with five types of analyses, i.e. analysis to understand the impacts of temperature distribution, reinforcement bars, an internal steel plate, and creep of mortar. The results show that cracking and delamination occur inside the CBS, resulting in a lack of cracking on the outside. They also show that the cracks are reduced by rebar and creep, resulting in cracks extending from the innermost edge to a depth of approximately 150 mm.
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