Kralios A C, Kralios F A, Anderson F L, Leonard M
Department of Veterans Affairs Medical Center, Cardiology Section, University of Utah, Salt Lake City 84148, USA.
J Mol Cell Cardiol. 1998 Feb;30(2):255-68. doi: 10.1006/jmcc.1997.0589.
Coronary venous hypertension induced by partial coronary sinus obstruction (CSO) in the dog, prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia. Also, CSO acting presumably through enhanced myocardial hydration, normalizes the inhomogenous extracellular potassium ([K+]o) accumulation, a major factor in producing the electrophysiological disparities, characteristic of arrhythmogenic substrate. To further clarify the mechanism of early ischemic VF prevention in dogs, radioactive microspheres were used to evaluate regional perfusion changes, resulting from CSO sufficient to raise the coronary sinus pressure to 40 mmHg, before and during ischemia induced by double coronary artery occlusion (CAO) (n=5). Also, global or regional unipolar electrogram mapping was used to assess changes of epicardial ventricular activation times (AT) and sequence and activation recovery intervals (ARI) during CSO, CAO and combined CSO and CAO, induced in random order (n=8). CSO did not affect regional perfusion nor improved collateral blood flow during ischemia. With CSO, AT shortened modestly over time (0.41+/-1.1 ms/min, r=0.85, P<0. 05) and ARI transiently decreased by up to 5.5%. With CAO, AT became variably delayed and isochrone map distortions were indicative of localized conduction delays or blocks, consistent with elevated [K+]o. In contrast, when CAO was preceded by CSO, AT delays were homogenous and normal activation sequence was preserved. Also, whereas with CAO, ARI shortened unequally over the ischemic region by as much as 43% at individual sites (average of 38.3+/-6.8 ms, P<0. 001), with combined CSO and CAO, ARI shortening was less pronounced and more homogenous (26.1+/-5.6 ms, P<0.05), not exceeding 29% at any site. Thus, in accordance with previous findings of enhanced [K+]o homogeneity, coronary venous hypertension reduces the disparities of activation and refractoriness of ischemia attributable, at least in part, to disparate [K+]o accumulation. Since no collateral blood flow improvement could be identified, the salutary electrophysiological effects of CSO may reflect a more homogenous extracellular environment, due to preservation of normal microvascular pressure (Pmv) and sustained filtration and lymph flow.
犬冠状动脉窦部分阻塞（CSO）所致的冠状静脉高压可预防或延缓急性缺血早期可预测的心室颤动（VF）。此外，CSO可能通过增强心肌水合作用，使不均匀的细胞外钾（[K+]o）蓄积正常化，而这种蓄积是产生电生理差异（致心律失常基质的特征）的主要因素。为进一步阐明犬早期缺血性VF预防机制，在双冠状动脉闭塞（CAO）诱导的缺血前后，使用放射性微球评估CSO使冠状窦压力升高至40 mmHg时的区域灌注变化（n = 5）。此外，采用整体或区域单极电图标测评估CSO、CAO以及随机顺序诱导的CSO与CAO联合作用期间的心外膜心室激活时间（AT）、激活顺序及激活恢复间期（ARI）的变化（n = 8）。CSO不影响缺血期间的区域灌注，也未改善侧支血流。存在CSO时，AT随时间适度缩短（0.41±1.1 ms/分钟，r = 0.85，P < 0.05），ARI短暂降低达5.5%。CAO时，AT出现不同程度延迟，等时线图变形表明存在局部传导延迟或阻滞，这与[K+]o升高一致。相反，若在CAO之前进行CSO，AT延迟是均匀的，且保留了正常激活顺序。此外，CAO时，缺血区域的ARI在各部位不均等地缩短多达43%（平均38.3±6.8 ms，P < 0.001），而CSO与CAO联合作用时，ARI缩短不那么明显且更均匀（26.1±5.6 ms，P < 0.05），在任何部位均未超过29%。因此，根据先前关于[K+]o同质性增强的研究结果，冠状静脉高压减少了缺血时激活和不应期的差异，这至少部分归因于不同的[K+]o蓄积。由于未发现侧支血流改善，CSO有益的电生理效应可能反映了由于正常微血管压力（Pmv）的维持以及持续的滤过和淋巴流而形成的更均匀的细胞外环境。
