Pagliaro P, Gattullo D, Merletti A, Losano G, Marsh N A
Department of Human Anatomy and Physiology University of Torino.
Boll Soc Ital Biol Sper. 1995 Mar-Apr;71(3-4):75-81.
In 5 anaesthetized vagotomized dogs the administration of an inhibitor of the synthesis of nitric oxide (NO) was seen to reduce the heart rate, although the arterial pressure was prevented from increasing. Such a finding suggests that the inhibition of nitric oxide release can produce bradycardia without the involvement of baroreceptor reflexes. Since NO inhibition is known to increase the concentration of adenosine in the myocardium, in 3 additional dogs, dipyridamole, which also potentiates the effect of adenosine, was infused: a reduction in heart rate was observed also in these animals. In both groups of animals, before and after the administration of the relevant compound, the increase in ABP obtained with aortic constriction caused the same reduction in heart rate, which which was attributed to a reduction of the basal sympathetic discharge, which was shown not to be affected by NO inhibition. It is concluded that NO inhibition can cause bradycardia without the intervention of any nervous mechanism but with the possible intervention of an increase in myocardial adenosine concentration.
在5只麻醉的迷走神经切断犬中，尽管动脉压未升高，但一氧化氮（NO）合成抑制剂的给药会使心率降低。这一发现表明，抑制一氧化氮释放可在不涉及压力感受器反射的情况下产生心动过缓。由于已知抑制NO会增加心肌中腺苷的浓度，因此在另外3只犬中，输注了也能增强腺苷作用的双嘧达莫：这些动物的心率也出现了降低。在两组动物中，在给予相关化合物之前和之后，主动脉缩窄引起的动脉血压升高导致心率出现相同程度的降低，这归因于基础交感神经放电的减少，且已表明基础交感神经放电不受NO抑制的影响。得出的结论是，抑制NO可在不涉及任何神经机制的情况下导致心动过缓，但可能是通过心肌腺苷浓度升高来实现的。
