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在离体灌注猪心脏急性局部缺血期间,细胞外钾离子浓度([K+]o)、跨壁电位(TQ电位)的异质性及心室颤动的诱发性。

Heterogeneities in [K+]o and TQ potential and the inducibility of ventricular fibrillation during acute regional ischemia in the isolated perfused porcine heart.

作者信息

Coronel R, Wilms-Schopman F J, Dekker L R, Janse M J

机构信息

Department of Experimental Cardiology, Academic Medical Center, Amsterdam, Netherlands.

出版信息

Circulation. 1995 Jul 1;92(1):120-9. doi: 10.1161/01.cir.92.1.120.

Abstract

BACKGROUND

The relation between the inducibility of ventricular fibrillation (VF) and heterogeneity of the extracellular potassium concentration ([K+]o) and of TQ potential is unknown.

METHODS AND RESULTS

Data from 78 epicardial DC electrodes or from up to 32 intramural K+ electrodes were acquired simultaneously. Induction of VF was attempted with one or two ventricular premature beats induced in normal myocardium in isolated porcine hearts during (1) regional perfusion of the left anterior descending artery (LAD) with a normoxic, hyperkalemic solution ([K+] 6 to 19.6 mmol/L), (2) simulated ischemia, ie, LAD perfusion with a glucose-free, hypoxic solution ([K+] 4 to 16 mmol/L, PO2 < 5 mm Hg, pH 6.98), and (3) regional ischemia produced by stopping LAD flow. During normoxic, hyperkalemic LAD perfusion, no VF could be induced (12 interventions, 7 hearts). During simulated ischemia (27 interventions), VF could be induced only when [K+]o was between 8 and 13.5 mmol/L. After 5 minutes of true regional ischemia, more sites with [K+]o between 8 and 13.5 mmol/L were present than after 10 minutes. VF could be induced with 1 ventricular premature beat in 11 of 17 interventions after 5 minutes and in 0 of 14 interventions after 10 minutes of ischemia (P < .001). Regional simulated ischemia presents a relatively homogeneous condition compared with 5 minutes of regional ischemia (SD +/- SEM of TQ potential in LAD tissue, 0.9 +/- 0.05 versus 2.1 +/- 0.13 mV, respectively). True ischemia superimposed on regional simulated ischemia caused the rapid development of heterogeneities in [K+]o and TQ potential and caused VF after 45 +/- 7 seconds in all interventions. Activation maps of induction of VF suggest a different mechanism of unidirectional block during simulated ischemia from that in true ischemia.

CONCLUSIONS

(1) In the presence of hypoxia and acidosis, [K+]o between 8 and 13.5 mmol/L provides the conditions necessary for the induction of VF; (2) after 5 minutes of ischemia, these conditions are present in a larger area and inducibility of VF is higher than after 10 minutes of ischemia; and (3) small heterogeneities within the intermediate K(+)-concentration domain (8 to 13.5 mmol/L) are associated with high inducibility of VF.

摘要

背景

室颤(VF)的可诱导性与细胞外钾浓度([K+]o)及TQ电位的异质性之间的关系尚不清楚。

方法与结果

同时采集78个心外膜直流电极或多达32个心内膜钾电极的数据。在以下情况下,尝试通过在离体猪心脏的正常心肌中诱发一或两个室性早搏来诱导VF:(1)用常氧、高钾溶液([K+] 6至19.6 mmol/L)对左前降支动脉(LAD)进行区域灌注;(2)模拟缺血,即使用无糖、低氧溶液([K+] 4至16 mmol/L,PO2 < 5 mmHg,pH 6.98)灌注LAD;(3)停止LAD血流导致的区域缺血。在常氧、高钾LAD灌注期间,无法诱导出VF(12次干预,7颗心脏)。在模拟缺血期间(27次干预),仅当[K+]o在8至13.5 mmol/L之间时才能诱导出VF。真正的区域缺血5分钟后,[K+]o在8至13.5 mmol/L之间的部位比缺血10分钟后更多。缺血5分钟后的17次干预中有11次用1个室性早搏可诱导出VF,缺血10分钟后的14次干预中则无1次成功(P <.001)。与5分钟的区域缺血相比,区域模拟缺血呈现出相对均匀的状态(LAD组织中TQ电位的标准差±标准误分别为:模拟缺血0.9±0.05 mV,区域缺血2.1±0.13 mV)。叠加在区域模拟缺血上的真正缺血导致[K+]o和TQ电位迅速出现异质性,并在所有干预中45±7秒后导致VF。VF诱导的激活图表明,模拟缺血期间单向阻滞的机制与真正缺血时不同。

结论

(1)在存在缺氧和酸中毒的情况下,[K+]o在8至13.5 mmol/L之间为诱导VF提供了必要条件;(2)缺血5分钟后,这些条件在更大面积存在,VF的可诱导性高于缺血10分钟后;(3)中等钾浓度域(8至13.5 mmol/L)内的小异质性与VF的高诱导性相关。

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