Schoenfeld W N, Kadden R M, McMillan J C
Pavlov J Biol Sci. 1977 Jan-Mar;12(1):32-40.
The functional relationship between heart rate, under atrial pacing, and the intensity of pacing pulses, was determined for intensities ranging from well below the complete heart rate capture threshold to suprathreshold intensities. A separate capture-intensity function was determined for each of the pacing frequencies 180, 240, 300 and 360 pulses per min, and then used to evaluate the effects of propranolol hydrochloride and atropine sulfate on atrial pacing. Propranolol resulted in an increase in the amount of current (mA) required to achieve a given degree of cardiac capture, whereas atropine resulted in a decrease. These shifts in the capture-intensity functions along the intensity axis were possibly caused by drug antagonism of beta-adrenergic and cholinergic receptors, respectively, although the effects might also have been due to modifications of the electrical responsivity of the cardiac muscle, independently of the neural blockade.
在心房起搏情况下,确定了心率与起搏脉冲强度之间的函数关系,起搏脉冲强度范围从远低于完全心率捕获阈值到超阈值强度。针对每分钟180、240、300和360次脉冲的每个起搏频率分别确定了单独的捕获强度函数,然后用于评估盐酸普萘洛尔和硫酸阿托品对心房起搏的影响。普萘洛尔导致实现给定程度心脏捕获所需的电流(毫安)量增加,而阿托品则导致电流减少。捕获强度函数沿强度轴的这些变化可能分别是由β-肾上腺素能受体和胆碱能受体的药物拮抗作用引起的,尽管这些影响也可能是由于心肌电反应性的改变,与神经阻滞无关。