Ventricular fibrillation resulting from ischemia at a site remote from previous myocardial infarction. A conscious canine model of sudden coronary death.

Ventricular fibrillation resulting from ischemia at a site remote from previous myocardial infarction. A conscious canine model of sudden coronary death.
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DOI:
10.1016/0002-9149(82)90484-2
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发表时间:
1982-12
期刊:
The American journal of cardiology
影响因子:
--
通讯作者:
E. Patterson;K. Holland;B. Eller;B. Lucchesi
E. Patterson;K. Holland;B. Eller;B. Lucchesi
中科院分区:
其他
文献类型:
--
作者:
E. Patterson;K. Holland;B. Eller;B. Lucchesi

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在麻醉的狗中,将30号银丝插入左回旋支(LC)冠状动脉的管腔中,通过随后闭塞左前降支(LAD)冠状动脉90分钟,然后通过临界狭窄再灌注来产生心肌缺血性损伤。急性心肌梗死后4天,犬自由活动,用150 μA阳极电流损伤LC冠状动脉内膜。在132 ± 65分钟(平均值±标准差[SD])时,冠状动脉血栓形成和随后的冠状动脉血流量减少伴有S-T段变化,在141 ± 60分钟时,30只犬中有29只(97%)发生室颤(VF)。LAD分布区的CT质量为左心室总质量的15 ± 8%,LC冠状动脉分布区无不可逆缺血性损伤的组织化学证据。VF之前LC冠状动脉分布内延迟电活动的发展,以及LC冠状动脉分布的心外膜下区域内持续局部电活动伴随的室性心律失常的发展。在10只犬中,在没有早期闭塞和再灌注的情况下,在LAD冠状动脉周围放置严重狭窄,LC内膜损伤和随后的血栓形成仅导致2例(20%)死于VF。因此,急性心肌缺血在一个网站远离以前的心肌梗死增加的可能性原发性VF在清醒的狗。这种冠状动脉猝死模型可以模拟人类的临床状态,并可能作为一个适当的模型,与VF的发展和潜在的抗心律失常药物的评价相关的电生理机制的研究。
In anesthetized dogs, a 30 gauge silver wire was inserted into the lumen of the left circumflex (LC) coronary artery and myocardial ischemic injury was produced by subsequent occlusion of the left anterior descending (LAD) coronary artery for 90 minutes followed by reperfusion through a critical stenosis. Four days after acute myocardial infarction, with the dog ambulatory, the intimai surface of the LC coronary artery was injured by applying a 150 μA anodal current. Coronary artery thrombosis and subsequent reduction in coronary artery blood flow were accompanied by S-T segment changes at 132 ± 65 minutes (mean ± standard deviation [SD]) with ventricular fibrillation (VF) occurring in 29 of 30 dogs (97% ) at 141 ± 60 minutes. Infarct mass in the LAD distribution was 15 ± 8% of total left ventricular mass with no histochemical evidence of irreversible ischemic injury in the LC coronary artery distribution. VF was preceded by the development of delayed electrical activity within the LC coronary artery distribution, and the development of ventricular arrhythmias accompanied by continuous local electrical activity within the subepicardial region of the distribution of the LC coronary artery. In 10 dogs with placement of a critical stenosis around the LAD coronary artery without earlier occlusion and reperfusion, LC intimal injury and subsequent thrombus formation resulted in only 2 deaths (20% ) from VF. Thus, acute myocardial ischemia at a site distant to a previous myocardial infarction enhances the likelihood of primary VF in the conscious dog. This model of sudden coronary death may simulate the clinical state in man and might serve as an appropriate model for the study of electrophysiologic mechanisms associated with the development of VF and for the evaluation of potential antifibrillatory drugs.