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β受体阻滞剂治疗期间迷走神经刺激对缺血心肌的有益作用。

Beneficial effects of vagal stimulation on the ischaemic myocardium during beta-receptor blockade.

作者信息

Kjekshus J K, Blix A S, Grøttum P, Aasen A O

出版信息

Scand J Clin Lab Invest. 1981 Jun;41(4):383-9. doi: 10.3109/00365518109092060.

DOI:10.3109/00365518109092060
PMID:7313522
Abstract

The effect of vagal stimulation on the myocardial ischaemia produced by acute coronary occlusion during beta-receptor blockade has been examined. Epicardial ST-segment elevation, myocardial surface temperature and regional blood flow were determined 10 min after coronary occlusion in the dog. Coronary occlusion after beta-receptor blockade alone raised the average ST-segment from 0.5 +/- 0.3 to 3.1 +/- 0.5 mV (SEM) (p less than 0.001). Subsequent vagal stimulation with beta-receptor blockade, which reduced heart rate from 129 to 50 beats/min, mean arterial pressure from 123 to 78 mmHg, but increased cardiac output from 1164 to 1855 ml/min, resulted in marked reduction in ST-segment elevation to 0.3 +/- 0.2 mV which was not different from the control before occlusion. Epicardial temperature was markedly decreased in the ischaemic area following coronary occlusion. The temperature difference between central ischaemic and surrounding areas became smaller after beta-receptor blockade, and vanished during vagal stimulation. Vagal stimulation caused a 55% decrease of blood flow in all non-ischaemic regions. A smaller reduction took place in the border zone where flow values close to those of the non-ischaemic myocardium were obtained. In the central ischaemic area blood flow remained unchanged despite the reduction in arterial pressure. Thus, vagal stimulation resulted in decreased collateral resistance in the ischaemic area and a marked reduction of myocardial oxygen requirement of both non-ischaemic and border zone myocardium, additional to that obtained with beta receptor blockade. The provision of energy to the ischaemic myocardium is therefore very favourably balanced with its actual demand during vagal stimulation.

摘要

研究了迷走神经刺激对β受体阻滞剂作用下急性冠状动脉闭塞所产生的心肌缺血的影响。在犬冠状动脉闭塞10分钟后,测定了心外膜ST段抬高、心肌表面温度和局部血流量。单独进行β受体阻滞剂处理后冠状动脉闭塞,使平均ST段从0.5±0.3mV升高至3.1±0.5mV(标准误)(p<0.001)。随后在β受体阻滞剂存在的情况下进行迷走神经刺激,心率从129次/分钟降至50次/分钟,平均动脉压从123mmHg降至78mmHg,但心输出量从1164ml/分钟增加至1855ml/分钟,结果ST段抬高显著降低至0.3±0.2mV,与闭塞前的对照值无差异。冠状动脉闭塞后,缺血区域的心外膜温度明显降低。β受体阻滞剂处理后,中央缺血区与周围区域的温差变小,在迷走神经刺激期间消失。迷走神经刺激使所有非缺血区域的血流量减少55%。在边缘区血流量减少幅度较小,此处获得的血流值接近非缺血心肌的血流值。尽管动脉压降低,但中央缺血区的血流量保持不变。因此,迷走神经刺激导致缺血区域的侧支循环阻力降低,非缺血区和边缘区心肌的心肌需氧量显著减少,这是在β受体阻滞剂处理基础上额外的减少。因此,在迷走神经刺激期间,缺血心肌的能量供应与其实际需求得到了非常有利的平衡。

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