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Objective To explore the molecular mechanism of prolonged atrial repolarization in rats with reperfusion atrial arrhythmia.Methods Sixteen Langendorff isolated heart perfusion models made by male SD rats were randomly divided into control group(group C,n = 8)and hypothermic ischemia-reperfusion group(group IR,n = 8).According to the occurrence of atrial arrhythmia after reperfusion,group IR was further subdivided into reperfusion non-atrial arrhythmia subgroup(group N-RAA)and reperfusion atrial arrhythmia subgroup(group R-AA).Group C was perfused with 37℃K-H solution for 120 min.In group IR,the isolated heart was perfused with 37℃K-H solution for 30 min and stopped,and the isolated heart was perfused with 4℃Thomas solution(20 mL/kg)for 60 mins.When the heart stopped for 30 mins,the isolated heart was perfused with a half dose of 4℃Thomas solution(10℃).During cardioplegia,the isolated heart was protected by low temperature Thomas solution(4℃),and then reperfused for 30 mins with 37℃K-H solution.The monophasic action potential(MAP)of the right atrium was recorded at balanced perfusion for 30 mins(T0),balanced perfusion for 105 mins in group C/reperfusion for 15 mins in group IR(T1)and balanced perfusion for 120 mins in group C/reperfusion for 30 min in group IR(T2);The duration of 50%and 90%repolarization of monophasic action potential(MAPD50 and MAPD90)was measured.After electrophysiological monitoring,the expression of Kir2.1 and CaMKⅡ in right atrium was detected by Western blot.Results Compared with T0,MAPD50 and MAPD90 at T1 and T2 were significantly prolonged in group R-AA(P<0.05),and MAPD90 at T1 and T2 in group R-NAA and group R-AA were significantly longer than those in group C(P<0.05).Compared with group R-NAA,MAPD50 and MAPD90 in group R-AA were significantly prolonged at T1 and T2(P<0.05).The results of Western blot showed that the expression of Kir2.1 in group R-NAA and group R-AA was significantly lower than that in group C(P<0.05),and that in group R-AA was significantly lower than that in group R-NAA(P<0.05).The expression of CaMKⅡ in group R-NAA and group R-AA was significantly higher than that in group C(P<0.05),and the expression of CaMKⅡ in group R-AA was significantly higher than that in group R-NAA.Conclusion The prolonged duration of atrial repolarization in rats with hypothermic ischemia-reperfusion atrial arrhythmia may be related to the down-regulation of Kir2.1 expression and the up-regulation of CaMKⅡ expression.
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Objective To investigate the efficacy and safety of transthoracic minimally invasive occlusion operation guided by transesophageal echocardiography for the treatment of congenital atrial or/and ventricular septal defects (ASD/VSD).Methods The clinical data of a total of 44 patients who underwent surgical occlusion operation from September 2013 to June 2015 were summarized.The whole course of occlusion procedure were dynamically monitored and guided by transesophageal echocardiography.All the patients were followed up regularly by electrocardiogram and echocardiograph.Results Among the 44 patients,43 patients(28 VSDs and 16 ASDs,including one patient suffered with VSD and ASD simultaneously)were occluded successfully,and the other patient with VSD who failed in the surgery was converted to open heart repair.The occlusion operations were finished within 22 to 48 min.The length of incision spaned from 2 to 4.5 cm.The ventilator was used for 1 to 5 hours.The total drainge volumes were recorded each patient from 0 to 50 mL.The postoperative hospitalization stay was 2 to 6 days,and all patients survived and were discharged.During the follow-up of 1 to 12 months, there was no cases with A-V conduction block,valve incompetent,cardiac arrhythmia and residual shunt of heart septel defect.Conclusion Transthoraic mini-invasive surgical occlusion of atrial and ventricular septal defects is a therapeutic method with less trauma,higher safety and feasiblity,faster recovery,and the short-term therapeutic effect is satisfying.