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Study On The Mechanisms Of Electrical And Cellular Remodeling And Prethrombosis State In Patients With Atrial Fibrillation

Posted on:2003-10-18Degree:DoctorType:Dissertation
Country:ChinaCandidate:X J XiaFull Text:PDF
GTID:1104360065460893Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Part I. Study of the expression changes of calcium_handing genes in Sarcoplamic Reticular in patients with Rheumatic Atrial FibrillationBackground: Recent studies have demonstrated that atrial electrical remodeling in atrial fibrillation (AF) is associated with intracellular calcium overload. However , the express changes of calcium-handling genes remain unclear.Objective: The study investigated the changes of the calcium_handing genes - Ca2+-ATPase( SERCA), Ryanodine and IP3-I receptors(RyR2 and IP3R1) expression in Sarcoplamic Reticular in order to explain the role of Calcium-overloading in initiation and maintenance of AF. Methods: 38 patients with mitrial stenosis undergoing open heart surgery were studied. l00mg tissue was obtained from the right appendage and the right atrium respectively. The messenger ribonucleic acid (mRNA) amount of the calcium-handing genes of Sarcoplamic Reticular was measured by reverse transcription-polymerase chain reaction (RT-PCR)and normalized to the mRNA levels of glyceraldehyde 3-phosphate dehydrogenase(GAPDH). Results: Down-regulation of SERCA in human AF; The longer the duration of AF,the more obvious is the down-regulation .Up- regulation of RyR2 and IP3R1 mRNA in human AF;The longer the duration of AF,the more obvious is the up-regulation .There were no difference between the right atriums and the right appendages.Druges have no effect in the express of Ca2+-handling genes. Conclusion: The down-regulation of SERCA, up- regulation of RyR2and IP3R1 mRNA in Sarcoplamic Reticular may have correlations with the initiation or with the maintenance of AF.
Keywords/Search Tags:Atrial fibrillation, electrical remodeling, Sarcoplamic Reticular Ca2+-ATPase(SERCA), Ryanodine receptor, IP3 receptor
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