Hoskins E J, Priola D V, Weiss G K
Circ Shock. 1978;5(4):393-406.
To determine whether vagal activity during myocardial ischemia functions to stabilize the heart, the left anterior descending coronary artery in dogs was occluded for periods of 3 1/2 minutes with and without concurrent vagal stimulation. Bipolar electrograms were measured from the surface of the canine left ventricle within and outside the regions of intended ischemia. Ischemia in the absence of vagal stimulation depressed both the electrogram amplitude and the upstroke velocity of the electrogram signal. Vagal stimulation significantly decreased the absolute magnitude of the ischemia-induced decrease of the electrogram signal, which indicates that it tended to stabilize the insulted heart. This stabilizing influence however, was seen only in the presence of adrenergic blockade with practolol. The vagal response was only partially blocked by atropine, whereas it was abolished by lidocaine. These results suggest that a vagally mediated stabilization of the ischemic canine ventricle can occur and is unmasked only in the absence of sympathetic neural activity.
为了确定心肌缺血期间迷走神经活动是否起到稳定心脏的作用，在有或无同时进行迷走神经刺激的情况下，将犬的左冠状动脉前降支闭塞3分半钟。在预期缺血区域内外的犬左心室表面测量双极电图。在没有迷走神经刺激的情况下，缺血会降低电图幅度和电图信号的上升速度。迷走神经刺激显著降低了缺血引起的电图信号下降的绝对幅度，这表明它倾向于稳定受损伤的心脏。然而，这种稳定作用仅在使用心得宁进行肾上腺素能阻断时才可见。迷走神经反应仅被阿托品部分阻断，而被利多卡因消除。这些结果表明，迷走神经介导的缺血犬心室稳定作用可以发生，并且仅在没有交感神经活动时才会显现出来。
