Chiba S, Furukawa Y, Kobayashi M
Jpn Heart J. 1978 Mar;19(2):263-70. doi: 10.1536/ihj.19.263.
Effects of cardioactive substances on the post-stimulation potentiation of atrial contractility were studied in 17 isolated, blood-perfused preparations of dogs. Maximum degree of the post-stimulation potentiation was obtained over approximately 3.5 Hz within 5-60 sec of stimulation. Each drug was administered directly into the cannulated sinus node artery of isolated atrium. An adequate dose of verapramil, manganese chloride, or pentobarbital which caused marked depression of contractility did not significantly suppress the post-stimulation potentiation in percent changes. The post-stimulation potentiation was not inhibited by continuous infusion of adenosine, which caused a negative inotropic effect. Tetrodotoxin, propranolol, or caffeine also never suppressed the post-stimulation potentiation but ouabain abolished it in the majority of cases.
在17个离体、血液灌注的犬心脏标本上研究了心活性物质对心房收缩力刺激后增强作用的影响。在刺激5 - 60秒内，约3.5Hz频率下可获得最大程度的刺激后增强作用。每种药物均直接注入离体心房的插管窦房结动脉。能引起明显收缩力抑制的维拉帕米、氯化锰或戊巴比妥的适当剂量，在百分比变化方面并未显著抑制刺激后增强作用。持续输注引起负性肌力作用的腺苷并未抑制刺激后增强作用。河豚毒素、普萘洛尔或咖啡因也从未抑制刺激后增强作用，但哇巴因在大多数情况下可消除该作用。
