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目的为探讨自主神经系统对在体家兔急性心肌梗死(AMI)后跨室壁3层心肌细胞有效不应期(ERP)离散度的影响。方法分别在基础和心肌梗死状态下,在交感神经和迷走神经刺激的过程中,用自制复合电极结合程序电刺激法测定家兔在体基础和梗死时心外膜心肌、中层心肌和心内膜心肌的ERP,并计算跨室壁ERP的离散度(TDERP)。结果在基础状态下,交感神经刺激能缩短3层心肌细胞的ERP,中层心肌细胞的ERP缩短最明显,TDERP由(21±17)ms增加到(30±16)ms(P<0.05);迷走神经刺激能延长3层心肌的ERP,心内膜心肌ERP增加明显,TDERP由(21±17)ms降低到(24±18)ms,差异无显著性。在AMI后30 min,交感神经刺激延长3层心肌细胞的ERP,其中中层心肌细胞的ERP增加最明显,与基础状态下交感刺激相比,TDERP由(30±16)ms增加到(38±11)ms(P<0.05);迷走神经刺激时TDERP为(21±13)ms,与基础状态(24±18)ms迷走刺激相比,TDERP无显著变化。结论AMI后,交感神经兴奋能增加TDERP;迷走神经兴奋对TDERP无显著影响。
Objective To investigate the effect of autonomic nervous system (CNS) on the effective non-refractory period (ERP) dispersion in three-layer cardiomyocytes after acute myocardial infarction (AMI) in rabbits. Methods In the process of sympathetic and vagal stimulation, basal and infarcted myocardium, middle myocardium and endocardial myocardium were detected by self-made composite electrode combined with programmed electrical stimulation ERP and calculate trans-wall ERP dispersion (TDERP). Results In the basal state, sympathetic stimulation shortened the ERP of three layers of cardiomyocytes, and the ERP shortening of the middle myocardial cells was the most obvious. The TDERP increased from (21 ± 17) ms to (30 ± 16) ms (P <0.05) Stimulation prolonged the level of ERP in three layers of myocardium, increased ERP in endocardial myocardium, and decreased the TDERP from (21 ± 17) ms to (24 ± 18) ms with no significant difference. At 30 min after AMI, sympathetic stimulation prolonged the ERP of three layers of cardiomyocytes, and the ERP of middle layer myocytes increased most significantly. Compared with the basal state, the TDERP increased from (30 ± 16) ms to (38 ± 11) ms ) ms (P <0.05). TDERP was (21 ± 13) ms in vagal stimulation, and TDERP had no significant change compared with 24 ± 18 ms in basal condition. Conclusions After AMI, sympathetic activation can increase TDERP; vagus nerve excitement has no significant effect on TDERP.