Reid J V, Bhagat C I
S Afr J Med Sci. 1975;40(4):117-31.
The transient decrease in coronary conductance and flow that is seen when the atria contract has been studied in 6 anaesthetized, open-chest dogs in heart block, paced via epicardial pacemaker leads. Left circumflex and anterior descending coronary flows were recorded via Doppler ultrasonic flow probes; aortic and left ventricular pressures and electrocardiogram were recorded simultaneously. The transient conductance and flow decrease in diastole were found from linear regression to be consistent with the left ventricular pressure rise caused by atrial contraction, in the case of the anterior descending coronary artery, which also showed no decrease in peak systolic conductance or flow when atria and ventricles contracted simultaneously. Circumflex conductance and flow were decreased by an atrial contraction to an extent greater than could be accounted for by the rise in left ventricular diastolic pressure. Peak circumflex flow and conductance were also decreased in systole, by 12 per cent, when atrial and ventricular contractions were exactly synchronous so that the atria could not discharge into the ventricles. The systolic effect and the excessive diastolic effect are ascribed to compression of atrial branches of the circumflex artery. This artrial compression mechanism accounted for 37-75 per cent of the effect of an atrial contraction on conductance in diastole. Values from 5 dogs of systolic and diastolic conductance changes due to atrial compression were linearly related. Calculation of atrial flow by applying this percentage to the transient flow decrease indicated that 17 per cent of circumflex diastolic flow was atrial, and that this percentage stayed constant throughout diastole.
在6只麻醉开胸、处于心脏传导阻滞状态并通过心外膜起搏导线进行起搏的犬身上，研究了心房收缩时冠状动脉传导和血流的短暂下降情况。通过多普勒超声血流探头记录左旋支和前降支冠状动脉血流；同时记录主动脉和左心室压力以及心电图。对于前降支冠状动脉，通过线性回归发现舒张期传导和血流的短暂下降与心房收缩引起的左心室压力升高一致，并且在心房和心室同时收缩时，其收缩期峰值传导或血流也未降低。左旋支的传导和血流因心房收缩而降低的程度大于左心室舒张压升高所能解释的程度。当心房和心室收缩完全同步以至于心房无法将血液排入心室时，左旋支的峰值血流和传导在收缩期也降低了12%。收缩期效应和过度的舒张期效应归因于左旋支动脉心房分支的受压。这种心房受压机制占心房收缩对舒张期传导影响的37% - 75%。5只犬因心房受压导致的收缩期和舒张期传导变化值呈线性相关。通过将该百分比应用于短暂血流下降来计算心房血流，结果表明左旋支舒张期血流的17%来自心房，并且在整个舒张期该百分比保持恒定。
