Chiba S, Simmons T W, Levy M N
Arch Int Physiol Biochim. 1976 Feb;84(1):81-8. doi: 10.3109/13813457609072349.
(1) Using isolated, blood-perfused atrium preparation of dogs, the effect of ischemia on sinus rate was studied in ten preparations. Cessation of atrial perfusion usually induced gradual deceleration of the sinus rate which was not blocked by atropine. Occasionally, brief and slight sinus acceleration was initially observed in three of ten atrium preparations. This positive chronotropic effect was not blocked by a beta-adrenoceptor blocking agent, propranolol. (2) In every preparation, just after release of occlusion, there was an initial profound sinus deceleration, occasionally followed by oscillatory changes in sinus rate. (3) The chronotropic response pattern induced by temporary occlusion and release of the sinus node artery was not influenced by propranolol, phenoxybenzamine or atropine treatment. (4) These results suggest that ischemia exerts its principal effect directly on the sino auricular node pacemaker cells, rather than on neighboring nerve endings.
(1) 利用犬的离体、血液灌注心房标本，在10个标本中研究了缺血对窦性心率的影响。停止心房灌注通常会导致窦性心率逐渐减慢，且阿托品不能阻断这种减慢。偶尔，在10个心房标本中有3个最初观察到短暂而轻微的窦性加速。这种正性变时作用不能被β-肾上腺素能受体阻滞剂普萘洛尔阻断。(2) 在每个标本中，刚解除阻塞后，最初都有显著的窦性减慢，偶尔随后会出现窦性心率的振荡变化。(3) 临时阻塞和松开窦房结动脉所诱导的变时反应模式不受普萘洛尔、酚苄明或阿托品处理的影响。(4) 这些结果表明，缺血的主要作用是直接作用于窦房结起搏细胞，而不是邻近的神经末梢。
