| Objective: To investigate the correlation between the expressions of protein andmRNA in ultra-rapid delayed rectifier potassium ion channel KV1.5of atrial myocytemembrane in atrial fibrillation rats and the significance of corresponding channelprotein changes in ion channel remodelling of atrial fibrillation，from which toexplore the potential mechanism of myocardial electrical remodelling in atrialfibrillation；At the same time,observing the changes of atrial tissue morphology of allrats to demonstrate the role and significance of atrial structure remodelling forinitiation and maintain in atrial fibrillation.Methods:25Sprague-Dawley(SD) rats were taken for experiment,the mean weightwas (217.64±7.02) grams, including13males and12females. All of them weredivided into two groups by randomly and the10rats in control group,the rests inexperimental group. To the experimental group,the rats were injected drugs by thecaudal vein according to0.1mL/100g (including CaCl210mg/mL, Ach66μg/mL)once a day and the total process continued one week to make moldels of atrialfibrillation; As the control group,the other rats were injected isovolumetricphysiological saline according to the same method as the experimental group. Beforeand after the experiment,the rats of two groups were tested electrocardiogramrespectively and the results were recorded. One week later,all of the rats were put todeath and50mg of atrial organization was taken from each of them. After extractingtotal RNA of specimen by homogenate reagent with cracking liquid RZ,its qualityanalysis was tested by electrophoresis and the purity and concentration were acquiredby ultraviolet spectrophotometer. Using reverse transcription polymerase chainreaction(RT-PCR) to amplificate the purpose gene and test the content of specimenDNA for analyzing the expression of corresponding mRNA; The rest of the atrialorganizations were put into the bottle full of amount20%formaldehyde liquidmarked already to be soaked and fixed. Using alcohol of different concentration todehydrate according to the conventional method, taking normal butanol to soak andusing paraffin embedding for immunohistochemical staining,making section specimen after using xylene to transparent processing in order to detect the expressionof atrial myocyte KV1.5proteins and the changes of atrial organization structure.Results:○1After injecting the mixture drug of acetylcholine and calcium chloride bytail vein of experimental group rats, atrial rhythm was characterized by the typicalatrial fibrillation：P waves were disappeared from electrocardiogram, replaced withsmall“f†waves of different sizes and shapes, and the distance of R-R intervals wereabsolutely irregular.○2There was an obviously statistical significance of the relativeratio in data for mean KV1.5mRNA between the atrial fibrillation group rats and thecontrol group ones[(0.613±0.040) VS (0.848±0.036), t=13.777, p＜0.01].○3There was an obviously statistical significance of the optical density value in datafor mean immunohistochemical protein of KV1.5between the atrial fibrillation grouprats and the control group ones [(0.0896±0.0048) VS (0.1109±0.0033), t=11.047，p＜0.01].4.Comparing with the tissue sections from atrial organization in both grouprats demonstrates that the atrial organization in experimental group of rats wasfractured in different level, including muscle solution, atrial myocytehypertrophy,inflammatory cell infiltration, focal necrosis as well as fibrous tissuehyperplasia for pathological changes; However,the control group rats, whoseepicardial atrial tissue samples were not incrassation, the myocardial fibers wereintegrity,without myocardial solidification or myocardial damage,the distances ofmyocardial cell were broadened, but the endocardiums were intact.Conclusions:○1The expression of both mRNA and protein of ultra-rapid delayedrectifier potassium channel in atrial fibrillation rats have down-regulated,and thechanges might be a kind of mechanism for compensation and protection,which makethe action potential effective refractory period duration of atrial muscle cell extendand the result was disadvantage to reentry of atrial fibrillation.○2The atrial myocytestructure of atrial fibrillation rats was remodelled significantly.This changes should bea result from ischemia and oxygen deficiency,Which cause myocardium injury andenhance atrial structure remodelling, decreased its function and make it change fromphysiological compensatory into pathological change.little by little, the atriumstructure turn into irreversible injured，which cause the disorder of myocardialelectrical seriously.○3Atrial fibrillation can enhance atrial structure remodelling, on other hand, structure remodelling make the atrial fibrillation happen and maintanceeasily, such mutual action and induction are disadvantage to recover atrium structureor its function,which leads to severe myocardial cell electric activity disorder in theend. |
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