ABSTRACT
Objective To investigate the expression of α-smooth muscle actin (α-SMA)in patients with valvular atrial fibrillation and study the relationship betweenα-SMA and atrial fibrosis in patients with valvular atrial fibrillation (AF).Methods For this study we enrolled 84 consecutive patients with rheumatic heart disease who were to receive cardiac surgery.The patients were divided into AF group (AF,n=39)and sinus rhythm group (SR, n=45).Their clinical data including baseline demographics,routine laboratory test and echocardiographics were collected before surgery.The right atrial tissue (0 .3-0 .5 cm3 )was disserted during the surgery.Right atrial fibrosis was observed by Masson staining.The mRNA expression ofα-SMA in atrial tissue were determined by Real-time quantitative PCR.Western blot was used to measure the protein expression ofα-SMA in atrial tissue.Results The two groups did not significantly differ in sex ratio,age,blood pressure,blood biochemical indicators or other aspects of medical history (P>0.05).However,left and right atrium diameters in AF group were significantly larger than those in SR group (P<0 .05 ).Masson staining suggested that collagen volume fraction and collagen content were significantly higher in AF group than in SR group (P<0 .05 ).The mRNA and protein expressions ofα-SMA in right atrial tissue were obviously higher in AF group than in SR group (coefficients P<0 .05 ).The mRNA and protein expressions ofα-SMA from right atrial tissue in the 84 patients were positively correlated with collagen content (coefficients of 0.587 and 0.607;P=0.029,0.014,respectively).Conclusion There is significant atrial fibrosis in patients with valvular atrial fibrillation,which is closely related to up-regulated expression ofα-SMA gene.
ABSTRACT
Objective:To investigate the expression of fibrillin-1 (FBN-1) in the atrium tissue of the patients with rheumatic heart valve disease complicated with atrial fibrillation(AF), and to explore its relationship with atrial fibrosis in the patients with valvular atrial fibrillation.Methods:Eighty-four consecutive patients with rheumatic heart valve disease underwent cardiac surgery were enrolled in this study.The patients were divided into AF group(n=39) and sinus rhythm group(SR group, n=45).The clinical data of patients were collected before operation.The right atrium tissue (0.3-0.5 mm3) was disserted during operation.The degrees of right atrial fibrosis of the patients in two groups were observed by Masson staining.Western blotting method was used to measure the protein expressions of FBN-1 in atrium tissue of the patients in two groups.Results:There were no significant differences in the gender ratio, age, blood pressure, blood biochemical indicators and other aspects of medical history between two groups(P>0.05);the diameters of left and right atrium of the patients in AF group were significantly larger than those in SR group(P<0.05).The Masson staining results showed that there was obvious fibrosis in AF group, and the collagen volume fraction and collagen level in AF group were significantly higher than those in SR group (P<0.05).The expression level of FBN-1 in right atrium tissue in AF group was obviously higher than that in SR group(P<0.05).The expression level of FBN-1 protein in right atrium tissue of the patients with valvular atrial fibrillation was positively correlated with the collagen level(r=0.544,P=0.021).Conclusion:There is obvious atrium fibrosis in the patients with valvular atrial fibrillation;it is closely related to the up-regulation of the expression of FBN-1 gene.
ABSTRACT
BACKGROUND: Vascular smooth muscle cell(VSMC) is one of the major cell components of vascular wall and its pathologic effects in atherosclerosis has been verified and recognized. How to inhibit VSMC proliferation and migration becomes one of the hotspots in the researches regarding the prevention of coronary heart disease(CHD).OBJECTIVE: To observe the impacts of diethyl-2, 6-diethyl-4-furny-1,4-dihydropyridine-3, 5-dicarboxylate(EFDP) on angiotensin Ⅱ (Ang Ⅱ)-induced VSMC proliferation.DESIGN: A randomized controlled study based on VSMC of rabbit' s thoracic aorta cultured in vitro.SETTING: Department of cardiology in a military medical university of Chinese PLA.MATERIALS: The study was conducted in the Laboratory of Cardiology of Xijing Hospital of the Fourth Military Medical University of Chinese PLA between August 2003 and June 2004. Five New Zealand rabbits were selected for the harvest of VSMC. Animal cells were randomly divided into control group, Ang Ⅱ group and Ang Ⅱ + EFDP group(EFDP group).METHODS: New Zealand rabbits were fed by high-fat food. Thoracic aorta was harvested for the separation and culture of VSMC after the injury in thoracic aorta intima by sacculus. The experiment introduced the cultured rabbit VSMC to observe the impacts of EFDP on VSMC DNA synthesis and its time effect during VSMC proliferation promoted by Ang Ⅱ by 3H-TdR method.MAIN OUTCOME MEASURES: 3H-TdR intensity of radio activity in cells of each group to display the DNA synthesis during VSMC proliferation process.RESULTS: Ang Ⅱ could promote the synthesis of rabbit VSMC DNA, which hit its peak at the 36th hour compared with that of control group(358. 00± 49.01 vs 272.42 ± 54.96, P ＜ 0. 01 ) . EFDP had significant inhibitive effects on Ang Ⅱ-induced VSMC proliferation, which also displayed a significant dose-dependent relationship, i.e. with the elevation of EFDP concentration, its inhibitive rate on VSMC proliferation also gradually increased. At the 36th hour, 78.40 μ mol/L of EFDP had more significant effect than that of 0. 08 μmol/L of EFDP(281.50 ± 15.28 vs 349. 25 ±32.10, P＜ 0. 05).CONCLUSION: EFDP can significantly inhibit Ang Ⅱ-induced rabbit VSMC proliferation with certain dose-effect dependency and time responses,which provides a theoretical gist for the primary rehabilitative prevention of atherosclerosis.
ABSTRACT
BACKGROUND: Angiotensin Ⅱ has been found to induce atrial electrical remodeling, which can be blocked or inhibited by allicin.OBJECTIVE: To study the effects of allicin on angiotensin Ⅱ-induced calcium channel current and intracellular free calcium concentration in human atrial myocytes.DESIGN: A randomized controlled study based on human atrial myocytes freshly isolated.SETTING: Cardiology department of a military medical university of Chinese PLA.METHODS: This study was carried out from June 2003 to June 2004 in the Laboratory of Cardiology Department, Xijing Hospital, the Fourth Military Medical University of Chinese PLA. Ten patients with congenital heart disease who underwent extracorporeal circulation surgery were included in the study. Among them, there were 6 males and 4 females with the average age of 15 ± 6 years. Tissue samples were taken from their right auricle and sent to the lab, where the atrial myocytes were freshly isolated. There were four co-administration of angiotensin Ⅱ (0. 1 μmol/L)and allicin(50 μmol/L).The conventional whole-cell configuration of the patch-clamp technique was used to detect membrane electric current of Ca2 + in L type. Confocal microscope was used with Fluo-3/AM as calcium indicator to detect changes of intracellular free calcium concentration immediately and 15 minutes after drug intervention, respectively.MAIN OUTCOME MEASURES: The peak density of electric current of Ca2 + in L type and alteration of fluoresence intensity of intracellular free calcium concentration.electric current of Ca2 + in L type in human atrial myocytes was significantly increased by angiotensin Ⅱ of 0. 1 μmol/L[( - 12. 77 ± 1. 61) vs ( -5.78affect electric current of Ca2+ in L type in human atrial myocytes group, the peak density of electric current of Ca2 + in L type was significantly lower than that in angiotensin Ⅱ group[ ( - 8.75 ± 0.97) pA/pF, P ＜ 0. 05 ].in angiotensin Ⅱ group was significantly higher than that in control and allicin groups[(2 610.1±112.6, (299.2±27.3)%; 653.9±42.5, 0;simultaneously with angiotensin Ⅱ, the alteration of intracellular fluoresence intensity was much lower than that in angiotensin Ⅱ group[ ( 1284.9 ± 85.2,(96.5±8.4)%;P ＜0.05].CONCLUSION: Allicin antagonizes angiotensin Ⅱ-induced increase in the peak density of electric current of Ca2+ in L type and intracellular calcium overload, which may relieve atrial electrical remodeling.
