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Effects of Pre- and Postconditioning on Arrhythmogenesis in the In Vivo Rat Model
被引:11
作者:
Kolettis, Theofilos M.
[1
,2
,3
]
Vilaeti, Agapi D.
[2
,3
,4
]
Tsalikakis, Dimitrios G.
[5
]
Zoga, Anastasia
[6
]
Valenti, Mesele
[2
,3
]
Tzallas, Alexandros T.
[7
]
Papalois, Apostolos
[2
,3
,8
]
Iliodromitis, Efstathios K.
[6
]
机构:
[1] Univ Ioannina, Sch Med, Ioannina 45500, Greece
[2] Cardiovasc Res Inst, Ioannina, Greece
[3] Cardiovasc Res Inst, Athens, Greece
[4] Univ Ioannina, Sch Med, Dept Cardiol, Ioannina 45500, Greece
[5] Univ Western Macedonia, Dept Engn Informat & Telecommun Computat Cardiol, Kozani, Greece
[6] Univ Athens, Dept Cardiol 2, Sch Med, Athens 11528, Greece
[7] Technol Educ Inst Epirus, Dept Informat & Telecommun Technol, Arta, Greece
[8] ELPEN Res Lab, Athens, Greece
关键词:
preconditioning;
postconditioning;
arrhythmia;
cytoprotection;
ACUTE MYOCARDIAL-INFARCTION;
MONOPHASIC ACTION-POTENTIALS;
HEART-RATE-VARIABILITY;
VENTRICULAR-ARRHYTHMIAS;
REPERFUSION ARRHYTHMIAS;
ISCHEMIA-REPERFUSION;
DECREASES;
TACHYARRHYTHMIAS;
SUSCEPTIBILITY;
FIBRILLATION;
D O I:
10.1177/1074248413482183
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
The antiarrhythmic potential of postconditioning in in vivo models remains poorly defined. We compared the effects of pre- and postconditioning on ventricular arrhythmogenesis against controls with and without reperfusion. Wistar rats (n = 40, 269 +/- 3 g) subjected to ischemia (30 minutes)-reperfusion (24 hours) were assigned to the following groups: (1) preconditioning (2 cycles), (2) postconditioning (6 cycles), or (3) no intervention and were compared with (4) nonreperfused infarcts and (5) sham-operated animals. Infarct size was measured, and arrhythmogenesis was evaluated with continuous telemetric electrocardiographic recording, heart rate variability indices, and monophasic action potentials (MAPs). During a 24-hour observation period, no differences in mortality were observed. Reperfusion decreased infarct size and ameliorated sympathetic activation during the late reperfusion phase. Preconditioning decreased infarct size by a further 35% (P = .0017), but only a marginal decrease (by 18%, P = .075) was noted after postconditioning. Preconditioning decreased arrhythmias during ischemia and early reperfusion, whereas postconditioning almost abolished them during the entire reperfusion period. No differences were noted in MAPs or in the magnitude of sympathetic activation between the 2 interventions. Compared to postconditioning, preconditioning affords more powerful cytoprotection, but both interventions exert antiarrhythmic actions. In the latter, these are mainly evident during the ischemic phase and continue during early reperfusion. Postconditioning markedly decreases reperfusion arrhythmias during a prolonged observation period. The mechanisms underlying the antiarrhythmic effects of pre- and postconditioning are likely different but remain elusive.
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页码:376 / 385
页数:10
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