在最大冠状动脉扩张期间，心房颤动引起的α受体收缩。

Alpha-receptor constriction induced by atrial fibrillation during maximal coronary dilatation.

作者信息

Ertl G, Wichmann J, Kaufmann M, Kochsiek K

出版信息

Basic Res Cardiol. 1986 Jan-Feb;81(1):29-39. doi: 10.1007/BF01907425.

DOI:10.1007/BF01907425

Abstract

The mechanism of coronary vasoconstriction induced by atrial fibrillation during maximal coronary dilatation was studied in 19 chloralose-urethane anesthetized dogs. Maximal coronary dilatation was achieved by carbochromene (5 mg/kg i.v.) or dipyridamole (0.2 mg/kg i.v.). Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Atrial fibrillation was compared with rhythmic atrial pacing at similar heart rates (207 +/- 12 vs. 204 +/- 12 beats/min). During maximal coronary dilatation, coronary resistance was 0.38 +/- 0.05 mm Hg X min X 100 g/ml (RU) at sinus rhythm, 0.41 +/- 0.06 RU at atrial pacing, and 0.52 +/- 0.07 RU at atrial fibrillation, that was significantly (p less than 0.005) higher than during sinus rhythm and atrial pacing. Accordingly, coronary oxygen extraction was 14 +/- 1% at sinus rhythm, 17 +/- 1% at atrial pacing (p less than 0.005 vs. sinus rhythm) and 27 +/- 2% at atrial fibrillation (p less than 0.001 vs sinus rhythm and atrial pacing). Beta-adrenoceptor blockade with propranolol (1 mg/kg i.v.) did not prevent this coronary vasoconstrictive effect. Following alpha-blockade with phenoxybenzamine (10 mg/kg i.v.), however, coronary resistance was 0.52 +/- 0.08 RU during sinus rhythm, 0.54 +/- 0.10 RU during atrial pacing and 0.57 +/- 0.09 RU during atrial fibrillation. The data suggest coronary vasoconstriction induced by atrial fibrillation mediated by an alpha-adrenoceptor mechanism.

摘要

在19只氯醛糖-乌拉坦麻醉的犬中研究了最大冠脉扩张时房颤诱发冠脉血管收缩的机制。通过静脉注射卡波铬烯（5mg/kg）或双嘧达莫（0.2mg/kg）实现最大冠脉扩张。用电磁流量计测量左旋冠脉血流量。将房颤与相似心率（207±12对204±12次/分钟）下的有节律心房起搏进行比较。在最大冠脉扩张时，窦性心律时冠脉阻力为0.38±0.05mmHg×min×100g/ml（RU），心房起搏时为0.41±0.06RU，房颤时为0.52±0.07RU，显著高于窦性心律和心房起搏时（p<0.005）。因此，窦性心律时冠脉氧摄取率为14±1%，心房起搏时为17±1%（与窦性心律相比p<0.005），房颤时为27±2%（与窦性心律和心房起搏相比p<0.001）。静脉注射普萘洛尔（1mg/kg）进行β-肾上腺素能受体阻滞不能预防这种冠脉血管收缩效应。然而，静脉注射苯氧苄胺（10mg/kg）进行α-受体阻滞后，窦性心律时冠脉阻力为0.52±0.08RU，心房起搏时为0.54±0.10RU，房颤时为0.57±0.09RU。数据提示房颤诱发的冠脉血管收缩由α-肾上腺素能受体机制介导。