| Objective: To investigate the effect of dexmedetomidine on monophasic action potential(MAP) and Cx43 expression in isolated rabbit hearts and to explore the mechanism for that effect on cardiac electrophysiologic stability.Methods: The effect of dexmedetomidine on monophasic action potential in all three layers of left ventricular:Langendorff isolated heart perfusion models were prepared with eighteen adult rabbits weighed 2.0-2.5kg after pentobarbital anesthetization.The hearts were randomly divided into three groups after perfusion in K-H solution for 15minutes(n=6): group C were perfused in K-H solution for 60 minutes, group L with25 ng/ml dexmedetomidine in K-H solution for 60 minutes and group H with 50ng/ml dexmedetomidine in K-H solution for 60 minutes.Heart rate,monophasic action potential amplitude(MAPA) and maximal velocity of 0 phase(Vmax) of three layers myocardial in left ventricular anterior wall were recorded at different time points in K-H solution perfusion for 15 min(T0) and additional perfusion for 15, 30, and 60min(T1-T3) respectively. 50%(MAPD50) and 90% of monophasic action potential duration(MAPD90) and transmural dispersion of repolarization were calculated.Early after depolarizations,delayed afterdepolarization and arrhythmia were also recorded.Research on the effect of dexmedetomidine on Cx43: left ventricle anterior wall was harvest after recording.Cx43 was detected immunohistochemically and also tested by Western blot. Results: 1, The effect of dexmedetomidine on monophasic action potential:(1).Intra-group comparison:Group H showed slower HR and prolonged MAPD50 and MAPD90 at T1-3 when compared with T0(P <0.05). Although TDR increased in group L(P <0.05),but had no statistical significance in HR, MAPD50 and MAPD90(P >0.05).Nor did MAPA and Vmax in all groups at each time points(P >0.05).(2)comparison among the groups:In comparison with group C,much slower HR,prolonged MAPD50 and MAPD90 and increased TDR showed in gruop H(P<0.05).When it comes to HR,MAPD50 and MAPD90 in group L, it, despite ofincreased TDR(P<0.05),was not statistically significant(P >0.05).Among these groups of,no statistical significance in MAPA and Vmax(P >0.05). 2,The effect of dexmedetomidine on Cx43 expression:there was no statistically significant difference between group L and group C in Cx43 expression,but the Cx43 distribution in group L tended to concentrate on lateral side of cardiomyocytes.A decreased expression of Cx43 was observed in group H when compared to other two groups and the large portion of Cx43 can be found on poles of these cells.Conclusion: Dexmedetomidine could increased TDR of three myocardium by down-regulating expression of gap junctional connexin and changing its distribution,which could result in an increased risk of arrhythmia. |
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