ABSTRACT
[Abstract ] Objective Modern pharmacological studies confirmed Zhigancao Decoction total extract, single active ingredients and their combinations could obviously inhibit arrhythmia.This study was to investigate the effects of Zhigancao Decoction medicated serum combined with myocardial tissue/silicon substrate microelectrode arrays (MEA) on rapid atrial pacing(RAP). Methods New Zealand white rabbits were randomly divided into normal control group, normal serum control group, Zhigancao Decoction medica-ted serum group and water decoction group, 8 in each group.After the establishment of an atrial fibrillation rabbit model, the field ac-tion potential duration ( fAPD) of the right atrial appendage ( RAA ) tissue was measured and the effections of Zhigancao Decoction medicated serum and water decoction on the fAPD of RAA were observed. Results The successful modeling of rapid atrial pacing induced atrial fibrillation in rabbits contributed to the significant shortening of fAPD 12 h after pacing compared to that before pacing ([174.30 ±1.36]ms vs[162.48 ±0.88]ms, P<0.05).After giving 10%~25% Zhigancao Decoction medicated serum and water decoction, the fAPDs of RAA tissue in rabbits with atrial fibrillation were prolonged, which represented positive dose-response relation-ship.The fAPDs of the rabbits given serum containing 10%, 15%, 20%and 25%Zhigancao Decoction were respectively (170.81 ± 0.61)ms, (171.00 ±0.46)ms, (179.08 ±0.67)ms, (179.76 ±2.26)ms, which were longer than those of water decoction group ([163.82 ±0.780]ms, [163.66 ±0.95]ms, [174.06 ±1.32]ms, [176.84 ±1.19]ms), and the difference was statistically sig-nificant (P<0.05). Conclusion The fAPD can be taken as one index of cardiac electrophysiological change, and 10%~25%Zh-igancao Decoction medicated serum can lead to fAPD extension in rabbit model of atrial fibrillation, which might be the electrophysio-logical mechanism of anti-atrial fibrillation.
ABSTRACT
<p><b>BACKGROUND</b>Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation (AF) was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF.</p><p><b>METHODS</b>Three groups of dogs were studied: adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL.</p><p><b>RESULTS</b>Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency.</p><p><b>CONCLUSION</b>These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AF.</p>
Subject(s)
Animals , Dogs , Age Factors , Apoptosis , Atrial Fibrillation , Atrial Remodeling , Connective Tissue Growth Factor , Physiology , Electrocardiography , Fibrosis , In Situ Nick-End Labeling , MicroRNAs , Physiology , Myocardium , PathologyABSTRACT
<p><b>OBJECTIVE</b>To observe the outcome and assess related factors affecting left atrial remodeling after percutaneous balloon mitral valvuloplasty (PBMV) in patients with mitral valve stenosis.</p><p><b>METHODS</b>From March 1998 to June 2002, there were 96 mitral valve stenosis patients who underwent PBMV in our hospital. Echocardiographic, 12 leads united electrocardiogram and other clinical datas were collected at preoperation, 1 week after operation, and 4 - 6 years after operation to retrospective analysis. Multiple stepwise regression analysis was used to assess controllable factors of left atrial remodeling.</p><p><b>RESULTS</b>Left atrial diameter reduced from (44.6 +/- 6.6) cm before PBMV to (42.8 +/- 6.5) cm (P > 0.05) 1 week after PBMV and enlarged to (47.2 +/- 5.7)cm (all P < 0.05) at the end of 4 - 6 years follow up post operation. The mitral valve area (MVA) increased from (1.06 +/- 0.32) cm2 before PBMV to (2.02 +/- 0.43) cm2 1 week after PBMV and (1.98 +/- 0.36) cm2 4 - 6 years post operation (all P < 0.05). Heart function assessed by NYHA classification improved significantly at 1 week and 4 - 6 years after surgery compared with pre-operation (P < 0.01). Multiple stepwise regression analysis showed that systolic blood pressure at 4 - 6 years after operation, MVA at 1 week after operation, preoperative atrial fibrillation, Wilkins score < or = 8, preoperative left atrial diameter were the independent predictive factors of left atrial remodeling at 4 - 6 years after PBMV.</p><p><b>CONCLUSIONS</b>PBMV was an effective therapy option for patients with mitral valve stenosis. Systolic blood pressure at 4 - 6 years after operation, MVA at 1 week after operation, preoperative atrial fibrillation, Wilkins < or = 8, preoperative left atrial diameter are the predictive factors of left atrial remodeling after PBMV.</p>