Zhao J, Billette J
Department of Physiology, Faculty of Medicine, University of Montreal, Quebec, Canada.
Am J Physiol. 1992 Jun;262(6 Pt 2):H1899-907. doi: 10.1152/ajpheart.1992.262.6.H1899.
The roles of changes in refractory and recovery properties of the atrioventricular node as affected by facilitation and fatigue in the genesis of Wenckebach periodicity were studied in isolated rabbit heart preparations. The contribution of nodal recovery time, facilitation, and fatigue to beat-to-beat changes in nodal conduction time (NCT) and effective (ERPN) and functional refractory periods of node (FRPN) occurring during stable 4:3 Wenckebach cycles was determined with premature stimulation protocols performed during these cycles. Fatigue prolonged, equally for each beat, NCT, ERPN, and FRPN, and therefore did not contribute to Wenckebach periodicity. Beat-to-beat increases in facilitation broadened the range of recovery times for which conduction was successful and decreased NCT, ERPN, and FRPN below the values expected from fatigue alone. However, ERPN and NCT increased overall from beat to beat because of NCT-induced (effects of NCT on ensuing refractoriness) increases in nodal refractoriness and consequent shortenings of the recovery time. These findings establish a complementary role for the recovery and refractory properties in generating the Wenckebach periodicity and demonstrate the modulating roles of facilitation and fatigue on this phenomenon.
在离体兔心标本中,研究了房室结不应期和恢复特性的变化在文氏周期发生过程中受易化和疲劳影响的作用。通过在稳定的4:3文氏周期期间执行的早搏刺激方案,确定了结恢复时间、易化和疲劳对在这些周期中发生的逐搏结传导时间(NCT)、有效(ERPN)和结功能不应期(FRPN)变化的贡献。疲劳对每个心动周期的NCT、ERPN和FRPN的延长作用相同,因此对文氏周期的产生没有贡献。逐搏易化的增加拓宽了成功传导的恢复时间范围,并使NCT、ERPN和FRPN低于仅由疲劳预期的值。然而,由于NCT诱导的(NCT对随后不应期的影响)结不应期增加和随之而来的恢复时间缩短,ERPN和NCT总体上逐搏增加。这些发现确立了恢复和不应期特性在产生文氏周期中的互补作用,并证明了易化和疲劳对这一现象的调节作用。