Wichmann J, Ertl G, Rudolph G, Kochsiek K
Basic Res Cardiol. 1983 Sep-Oct;78(5):473-91. doi: 10.1007/BF01906459.
The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2-7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n = 10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78 +/- 6 vs. 75 +/- 5 ml/min X 100 g) while coronary vascular resistance (CVR) (1.16 +/- 0.05 vs. 0.87 +/- 0.07 [m Hg X min X 100 gl/ml [RU], p less than 0.0001) and sinus oxygen saturation (26 +/- 2 vs. 22 +/- 1%, p less than 0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311 +/- 48 vs. 205 +/- 30 ml/min X 100 g, p less than 0.01) and coronary sinus oxygen saturation (65 +/- 6 vs. 42 +/- 6%, p less than 0.01), while CVR (0.27 +/- 0.03 vs. 0.37 +/- 0.04 RU, p less than 0.0001) was 38 +/- 8% (p less than 0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n = 11), CBF (92 vs. 125 +/- 14 ml/min X 100 g, p less than 0.001) and sinus oxygen saturation (24 +/- 2 vs. 30 +/- 2%, p less than 0.0025) were higher and CVR (1.16 +/- 0.11 vs. 0.97 +/- 0.10 RU, p less than 0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233 +/- 24 vs. 168 +/- 16 ml/min X 100 g, p less than 0.0005) and sinus oxygen saturation (70 +/- 3 vs. 57 +/- 2%, p less than 0.0005), while CVR (0.25 +/- 0.02 vs. 0.46 +/- 0.02 RU, p less than 0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.
在21只麻醉开胸犬身上研究了房颤对冠脉循环的影响。通过在左心耳局部应用乙酰胆碱（10%生理盐水溶液）或电刺激（2 - 7伏、2毫秒、50赫兹）诱发房颤。诱发房颤时（n = 10），平均主动脉压下降，心率显著升高；冠脉血流量（CBF）保持不变（78±6 vs. 75±5毫升/分钟×100克），而冠脉血管阻力（CVR）（1.16±0.05 vs. 0.87±0.07 [毫米汞柱×分钟×100克/毫升][阻力单位]，p < 0.0001）和窦氧饱和度（26±2 vs. 22±1%，p < 0.05）降低。静脉注射卡波铬（5毫克/千克，3分钟内）使冠脉最大程度扩张后，房颤导致CBF降低（311±48 vs. 205±30毫升/分钟×100克，p < 0.01）和冠脉窦氧饱和度降低（65±6 vs. 42±6%，p < 0.01），而CVR（0.27±0.03 vs. 0.37±0.04阻力单位，p < 0.0001）在房颤时比窦性心律时高38±8%（p < 0.0005）。当心脏起搏至与房颤时平均心率相同的速率时（n = 11），CBF（92 vs. 125±14毫升/分钟×100克，p < 0.001）和窦氧饱和度（24±2 vs. 30±2%，p < 0.0025）高于房颤时，CVR（1.16±0.11 vs. 0.97±0.10阻力单位，p < 0.0005）低于房颤时；在卡波铬使冠脉最大程度扩张时，起搏也导致更高的CBF（233±24 vs. 168±16毫升/分钟×100克，p < 0.0005）和窦氧饱和度（70±3 vs. 57±2%，p < 0.0005），而CVR（0.25±0.02 vs. 0.46±0.02阻力单位，p < 0.0005）低于房颤时。因此，房颤导致冠脉血管阻力降低，但冠脉氧摄取增加。当心率得到控制时，房颤的血管收缩作用就会显现出来。房颤时的冠脉血管收缩在冠脉最大程度扩张时似乎比对照时更明显。
