Szekeres L, Papp J G, Szilvássy Z, Udvary E, Vegh A
Institute of Pharmacology, A Szent-Györgyi Medical University, Szeged, Hungary.
Cardiovasc Res. 1993 Apr;27(4):593-6. doi: 10.1093/cvr/27.4.593.
The aim was to investigate whether moderate ischaemic stress induced by brief periods of cardiac pacing to twice the normal heart rate protects the heart from the electrophysiological and haemodynamic consequences of subsequent periods of rapid pacing.
Conscious rabbits with implanted right ventricular electrodes and a permanent catheter in the left ventricular cavity were studied. Hearts were paced at a rate of 500.min-1 for 5 min. The resulting transient ST segment elevation in intracavital electrogram, the ventricular effective refractory period, and the left ventricular end diastolic pressure were measured.
After discontinuation of pacing, a shortlasting ST segment elevation appeared in the endocardial electrogram, together with a transient rise in left ventricular end diastolic pressure. These changes were significantly reduced after a second pacing, provided that this was applied not later than 30 min after the first pacing; maximum protection occurred when there was a 5 min interval between these pacing periods. Serial stimulation (10 pacing periods with a 5 min interval between each) gave a similar protection to that resulting from a single pacing period. The protection was lost after 1 h; however, 24 h and 48 h (but not 72 h) after the end of serial stimulation there was again a reduction in postpacing ST segment and left ventricular end diastolic pressure elevation. At these times the ventricular effective refractory period was prolonged. The cyclo-oxygenase inhibitor sodium meclofenamate (1-2 mg.kg-1) prevented the early protection.
The results suggest that brief periods of rapid pacing induce both short term and long term cardioprotection, as shown by reduced electrophysiological and haemodynamic consequences of subsequent pacing periods. Endogenous prostanoids might play a role in the short term cardioprotection.
研究通过将心率短暂起搏至正常心率的两倍所诱导的适度缺血应激是否能保护心脏免受随后快速起搏时期的电生理和血流动力学影响。
对植入右心室电极且在左心室腔内置有永久导管的清醒家兔进行研究。以500次/分钟的速率起搏心脏5分钟。测量由此产生的腔内心电图中短暂的ST段抬高、心室有效不应期以及左心室舒张末期压力。
起搏停止后，心内膜心电图中出现短暂的ST段抬高，同时左心室舒张末期压力短暂升高。如果在第一次起搏后不迟于30分钟进行第二次起搏，这些变化会显著减轻；当两次起搏之间间隔5分钟时，保护作用最大。连续刺激（每次间隔5分钟进行10次起搏）产生的保护作用与单次起搏产生的保护作用相似。1小时后保护作用消失；然而，在连续刺激结束后24小时和48小时（但72小时未出现），起搏后ST段和左心室舒张末期压力升高再次降低。此时心室有效不应期延长。环氧化酶抑制剂甲氯芬那酸钠（1 - 2毫克/千克）可阻止早期保护作用。
结果表明，短暂的快速起搏可诱导短期和长期的心脏保护作用，后续起搏时期的电生理和血流动力学影响减轻即表明了这一点。内源性前列腺素可能在短期心脏保护中发挥作用。
