Cinca J, Worner F, Bardají A, Salas-Caudevilla A, Soler-Soler J
Servicio de Cardiología, Hospital General Valle de Hebrón, Barcelona, Spain.
Cardiovasc Res. 1991 Jul;25(7):586-93. doi: 10.1093/cvr/25.7.586.
The aim was to test the hypothesis that chronic sympathetic denervation of the boundaries of a healed myocardial infarction may modify the arrhythmogenic response to programmed electrical stimulation.
Electrical induction of ventricular arrhythmias and infarct size were evaluated in a control group of pigs with a one month old myocardial infarction induced by ligature of the left anterior descending coronary artery below the first diagonal branch. These were compared with a group of similarly infarcted pigs subjected to regional denervation of the peri-infarction area induced by topical pericoronary application of phenol. Denervation was verified by the absence of adrenergic histofluorescent reaction to glyoxylic acid in myocardial samples.
24 pigs (weight 15-20 kg) with myocardial infarction were studied, 13 of which were subjected to regional peri-infarction denervation, and 11 acted as controls.
Programmed ventricular stimulation with one to four extrastimuli at 500 and 400 ms basic cycle length at the left and right ventricles induced fewer episodes of ventricular fibrillation in the denervated than in the non-denervated group (five episodes in three pigs v 14 in nine pigs, p less than 0.005), but more episodes of sustained ventricular tachycardia (79 in eight pigs v 23 in two, p less than 0.001). Unlike fibrillation, induction of ventricular tachycardia increased with multiple extrastimuli and with short basic cycle length. The denervated preparations tended to develop smaller infarcts but this difference was not statistically significant: infarct weight (g) relative to total ventricular mass (g) = 7.2 (SD 2.4)% v 10.5(4.5)%.
Neural integrity of the non-ischaemic myocardium bordering a healed infarction modulates inducibility of ventricular tachycardia and fibrillation during programmed ventricular stimulation.
旨在验证以下假设,即对愈合心肌梗死边界进行慢性交感神经去神经支配可能会改变对程序性电刺激的致心律失常反应。
在一组通过结扎第一对角支下方的左前降支冠状动脉诱导出一个月陈旧性心肌梗死的猪中,评估室性心律失常的电诱导情况和梗死面积。将这些猪与另一组通过冠状动脉周围局部应用苯酚诱导梗死周围区域去神经支配的类似梗死猪进行比较。通过心肌样本中对乙醛酸无肾上腺素能组织荧光反应来证实去神经支配。
对24只患有心肌梗死的猪(体重15 - 20千克)进行了研究,其中13只接受了梗死周围区域去神经支配,11只作为对照。
在左、右心室以500和400毫秒的基础周期长度进行一至四个额外刺激的程序性心室刺激,去神经支配组诱发心室颤动的发作次数少于未去神经支配组(3只猪发作5次,9只猪发作14次,p < 0.005),但持续性室性心动过速的发作次数更多(8只猪发作79次,2只猪发作23次,p < 0.001)。与颤动不同,室性心动过速的诱发随着多个额外刺激和较短的基础周期长度而增加。去神经支配的标本梗死面积往往较小,但这种差异无统计学意义:梗死重量(克)相对于心室总质量(克) = 7.2(标准差2.4)%,对照组为10.5(4.5)%。
愈合梗死周围非缺血心肌的神经完整性在程序性心室刺激期间调节室性心动过速和颤动的诱发性。