White C W, Kerber R E, Weiss H R, Marcus M L
Circ Res. 1982 Aug;51(2):205-15. doi: 10.1161/01.res.51.2.205.
To study whether atrial fibrillation might produce local changes in the atrium which could facilitate the tendency of this arrhythmia to become chronic and self-perpetuating, we compared the effect of atrial fibrillation, atrial pacing, and acute volume loading on the perfusion and oxygen consumption of the atrium in anesthetized dogs. Measurement of atrial perfusion with microspheres indicates that during atrial fibrillation, atrial blood flow increases 2- to 3-fold. Right atrial pacing is a significantly less potent metabolic stimulus for atrial vasodilation. Using Doppler velocity recordings of sinus node artery blood flow velocity, a marked increase in velocity is observed within 5 seconds after the initiation of atrial fibrillation. During atrial fibrillation, the sinus node artery reactive hyperemia response is markedly attenuated. Atrial fibrillation acutely decreases atrial distensibility; atrial pressure increased 81 +/- 19% with only a small increase (9.7 +/- 3%) in atrial diameter measured by echocardiography. During sinus rhythm, volume expansion to equivalent levels of atrial pressure as seen during atrial fibrillation increased atrial diameter 21 +/- 5% P less than 0.05. Atrial oxygen consumption determined by the microspectrophotometric method markedly increases during atrial fibrillation, compared to control conditions (12.3 +/- 2.8 vs. 3.9 +/- 0.6 ml O2/min per 100 g, respectively) P less than 0.05. Atrial O2 extraction was 5.5 +/- 0.4 ml O2/ml blood in the control state, and did not change with interventions. There was a linear relationship between left atrial O2 consumption and blood flow in all experimental conditions. Atrial fibrillation therefore alters atrial hemodynamics and metabolism by increasing atrial blood flow and oxygen consumption and decreasing atrial distensibility. Since atrial perfusion during atrial fibrillation is high and atrial flow reserve is limited, it is possible that additional atrial metabolic requirements might lead to atrial ischemia, fibrosis, and, thereby, perpetuation of the arrhythmia.
为研究心房颤动是否会在心房产生局部变化，进而促使这种心律失常倾向于转变为慢性且自我持续存在，我们比较了心房颤动、心房起搏及急性容量负荷对麻醉犬心房灌注和氧消耗的影响。用微球测量心房灌注表明，在心房颤动期间，心房血流量增加2至3倍。右心房起搏对心房血管舒张而言是效力明显较弱的代谢刺激。利用窦房结动脉血流速度的多普勒速度记录，在心房颤动开始后5秒内可观察到速度显著增加。在心房颤动期间，窦房结动脉反应性充血反应明显减弱。心房颤动会急性降低心房顺应性；心房压力增加81±19%，而通过超声心动图测量的心房直径仅小幅增加（9.7±3%）。在窦性心律期间，将容量扩充至与心房颤动时所见相当的心房压力水平，心房直径增加21±5%，P<0.05。与对照状态相比，通过显微分光光度法测定的心房颤动期间心房氧消耗显著增加（分别为12.3±2.8与3.9±0.6 ml O2/分钟每100克），P<0.05。在对照状态下，心房氧摄取为5.5±0.4 ml O2/毫升血液，且干预后未发生变化。在所有实验条件下，左心房氧消耗与血流量之间呈线性关系。因此，心房颤动通过增加心房血流量和氧消耗以及降低心房顺应性来改变心房血流动力学和代谢。由于心房颤动期间心房灌注较高且心房血流储备有限，额外的心房代谢需求可能会导致心房缺血、纤维化，从而使心律失常持续存在。
