Elharrar V, Foster P R, Jirak T L, Gaum W E, Zipes D P
Circ Res. 1977 Jan;40(1):98-105. doi: 10.1161/01.res.40.1.98.
Changes in the ventricular diastolic excitability threshold following occlusion of the left anterior descending coronary artery (LAD) were studied in open-chest anesthetized dogs by using a new automatic threshold-following pacemaker (ATFP). The ATFP measures the diastolic excitability threshold by successively decreasing the duration of regularly occurring pacing stimuli until the ventricle fails to respond. Under control conditions, the threshold stimulus duration was 60 +/- 4 (mean +/- SEM) musec. In the first 1-3 minutes following occlusion of the LAD, the diastolic excitability threshold in the ischemic zone (IZ) decreased to 51 +/- 5 musec and then rapidly increased to 600 musec at 5 minutes. The initial decrease in excitability threshold at IZ could be abolished by elevating the serum K+ concentration prior to the LAD occlusion. These changes in excitability threshold at IZ could be prevented by infusing nonoxygenated solutions into the LAD at a site distal to the occlusion. As the excitability threshold increased in IZ during ischemia, the earliest time at which IZ could be reactivated by a stimulus with a voltage equal to twice the preligation diastolic voltage threshold was increased. In nine of 16 dogs, after 5 minutes of LAD ligation, the IZ to normal zone (NZ( activation time (when stimulating at IZ) exceeded the NZ to IZ activation time (when stimulating at NZ) by an average of 9 msec. We also found that in four dogs the NZ to IZ activation time exceeded the IZ to NZ activation time by an average of 10 msec. We conclude from these findings that a gradient of increasing excitability threshold exists as one moves from normally perfused toward more ischemic tissue, passing through a heterogenous border zone that manifests some areas which have a decreased excitability threshold and other areas which have an increased excitability threshold, and that these changes in excitability importantly influence the determination of refractory period durations and conduction times.
采用新型自动阈值跟踪起搏器（ATFP），在开胸麻醉犬身上研究了左前降支冠状动脉（LAD）闭塞后心室舒张期兴奋性阈值的变化。ATFP通过连续缩短规则出现的起搏刺激持续时间，直至心室无反应，来测量舒张期兴奋性阈值。在对照条件下，阈值刺激持续时间为60±4（均值±标准误）毫秒。在LAD闭塞后的最初1 - 3分钟内，缺血区（IZ）的舒张期兴奋性阈值降至51±5毫秒，然后在5分钟时迅速升至600毫秒。在LAD闭塞前升高血清钾浓度可消除IZ处兴奋性阈值的初始下降。通过在闭塞部位远端向LAD输注非氧合溶液，可预防IZ处兴奋性阈值的这些变化。随着缺血期间IZ处兴奋性阈值升高，用等于结扎前舒张期电压阈值两倍的电压刺激使IZ重新激活的最早时间延长。在16只犬中的9只，LAD结扎5分钟后，IZ至正常区（NZ）的激活时间（在IZ刺激时）比NZ至IZ的激活时间（在NZ刺激时）平均长9毫秒。我们还发现，在4只犬中，NZ至IZ的激活时间比IZ至NZ的激活时间平均长10毫秒。从这些发现我们得出结论，当从正常灌注组织向更缺血组织移动时，存在兴奋性阈值升高的梯度，经过一个异质边界区，该区域表现出一些兴奋性阈值降低的区域和其他兴奋性阈值升高的区域，并且这些兴奋性变化重要地影响不应期持续时间和传导时间的测定。
