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Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectinlike domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema. Abbreviations:-tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNFR1); TNF receptor type 2 (TNF-R2);

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Background:-Sometime, it's difficult to distinguish the electrophysiological mechanism of some tachycardia, and so, influencing the efficacy and safety of ablation operation. Therefore, it's helpful to analysis some tachycardia in particular mechanism, as in this case. Methods and results:-A 49 years old Chinese male patient had a history of paroxysmal palpitation for 25 years, and recurred more frequently in the month before admission. Electrocardiogram (ECG) showed no abnormity under sinus rhythm, and showed no specific sign to distinguish its reentrant mechanism when tachycardia running. Electrophysiological examination and the result of successful ablation showed that the retrograde pathway of its reentry was in slow conduction, and from which the reentry started; moreover, after partially ablating, the reentry started from antegrade slow conduction. Conclusion:-Careful cardiac electrophysiological examination and paying more attention to inducing conditions of tachycardia are critical to accurately determining the tachycardia mechanism.

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Background:-The Yellow Oleander is an ornamental tree that is common throughout the tropics. Ingestion of its seeds results in a clinical picture similar to digoxin toxicity. Objectives:-The aim of this study was to evaluate cardiac findings in acute Yellow Oleander poisoning. Methods and Materials: -A total of 21 patients with history of Yellow Oleander ingestion were enrolled in this study. Results:-All symptomatic patients had conduction defects affecting the sinus node, theatrio-ventricular node or both. Patients showing cardiac arrhythmias that required specific management had significantly higher serum potassium concentrations. Conclusion: -Most of the symptomatic patients had conduction defects affecting sinus or atrio-ventricular nodes but few had atrial or ventricular arrhythmias typical of digoxin poisoning.

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Arrhythmia is a big headache for cardiologist for a long time. A new antiarrythmic drug with good effects and few side effects should be explored. Hydrogen sulfide, a newly found gaseous transmitter, was found to have multi-effects on a variety of ion channels. It may be a promising antiarrythmic drug. This article reviews the different effects of hydrogen sulfide on different ion channels.

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Background-Electrical heterogeneity of the right ventricular outflow tract (RVOT) is regarded as one of the main electrophysiological substrates for Brugada syndrome. Recently quinidine has shown efficacy in patients with Brugada syndrome due to its ability to inhibit potassium current especially 4-aminopyridine-sensitive, non-Ca ²⁺ -dependent transient outward potassium current (Ito). However, much less is known on how extent quinidine in clinical therapeutic concentration range can inhibit this kind of electrical heterogeneity of RVOT Ito. Methods and Results-Single RVOT free wall epicardial (Epi) cell, midmyocardial (M) cell and endocarcial (Endo) cells were used for whole-cell voltage clamping and Ito was recorded at 37°C, 0.2 Hz depolarization pulse. Evident Ito tranmural heterogeneity existed in RVOT free wall. Under the condition of baseline, of 10 μM quinidine perfusion 5 minutes (mins), and of 10 ìM quinidine perfusion 7-10 mins, from 0 mV to 70 mV the whole transmural average Ito values of RVOT free wall were 10.2 pA/pF, 5.5 pA/pF and 3.5 pA/pF, respectively (between groups, P<0.01). The inhibitory percentage of 10 ìM quinidine at 5 mins and 7-10 mins steady-state level on the the whole Ito transmural heterogeneity of RVOT free wall were 46.3%±6% and 66.5%±11%, respectively. Conclusions-There exists a robust Ito transmural electrical heterogeneity in RVOT free wall and quinidine in clinical therapeutic concentration can depress this kind of heterogeneity effectively.

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Objective :-This study is to explore the effect of valsartan-eluting stents on neointima formation after stenting and to elucidate possible mechanisms how locally used valsartan prevents in-stent restenosis (ISR). METHOD: valsartan- and carriereluting stents were manufactured by using multi-layer-coated technology. Bare stents, carrier-eluting stents and valsartan- eluting stents were implanted into the abdominal aortas of the rabbits respectively. Quantitative angiography (QA) before, immediately after and 3 months after stent implantation were compared between the groups of bare (n=8), carrier-eluting (n=8) and valsartan-eluting stent (n=10), which allows the comparison of vascular diameters of aortas as well as indices of vascular neointimal formation, i.e. luminal area (LA), neointimal area (NIA), inner elastic membrane luminal area (IELA) and the maximal inner-membrane thickness (MIT) in 15 rabbits. α-Actin protein expression were detected by Envision two-step immunohistochemistry. Mean positive indices (MPI) of the above protein were analyzed semi-quantatively by IMS(Information Management System) cell image analysis system. MPI=positive area×OD (optical density). Collagen deposition in neointima was observed through MASSON stain among the three groups. Result:-the mean aortic diameters were similar in the three groups:bare stents group(n=8), carrier-eluting stents group(n=8) and valsartan eluting stents group(n=10) measured by QA at different time. A larger luminal area and a less neointimal hyperplasia in valsartan eluting-stents group was found compared with the other two groups. The mean luminal areas were 4345548±125822um2; 4302061±167952 um2; 5016269±207934um2 respectively. The mean neointimal areas were 1119635±163503um2; 1135636±136555um2; 441577±74099um2 and the mean maximal inner-membrane thickness were 210±30um;192±21um; 116±12um respectively. á-Actin protein expression was significantly lower in neointima of valsartan eluting-stents group than the other two groups. Through MASSON stain we found that Collagen was much richer in neointima of bare stents group and carrier-eluting stents group than valsartan eluting-stents group. Conclusion:-Valsartan eluting-stents inhibited neointimal hyperplasia after stenting by decreasing collagen deposition and smooth muscle cell proliferation. Therefore it would be potentially effective in preventing in-stent restenosis. Abbreviations:-Quantitative angiography (QA), luminal area (LA), neointimal area (NIA), inner elastic membrane luminal area (IELA), the maximal inner-membrane thickness (MIT), Mean positive indices (MPI), optical density (OD), Drugeluting stents (DES), in-stent restenosis(ISR), percutaneous transluminal coronary angioplasty (PTCA), angiotensin α type 2 receptor (AT2).

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Background-- Previous studies have shown that there is a circadian variation in the incidence of acute myocardial infarction. The aim of this study is to examine the circadian rhythms of acute myocardial infarction in patients with type 2 diabetes. Methods and Results-1016 consecutive patients admitted to a coronary care unit with acute ST elevation myocardial infarction were studied from January 2004 to December 2008. All patients were divided into two groups according to with or without diabetes. Admission rates were calculated according to the 6-hour interval of the day (circadian rhythm). The data were analyzed for variations within subgroups. In diabetic group, number of patients in the first to fourth quarters was 38, 45, 43, 46 respectively (NS). The corresponding figures for the controls were 174, 295, 183, 192 (P<0.01). The difference between the two groups was significant (P<0.02). Conclusion-There is no a significant circadian variation in the onset of acute myocardial infarction in diabetic subjects.

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