Chiba S, Simmons T W, Levy M N
Jpn Heart J. 1976 Sep;17(5):656-62. doi: 10.1536/ihj.17.656.
Using an isolated, blood-perfused atrium preparation, the effects of temperature on SA nodal pacemaker activity were investigated in 9 preparations. The PP interval decreased as temperature was raised. Regular sinus rhythm and atrial contraction were maintained above approximately 26 degrees C. Below 26 degrees C, sinus depolarization still showed a regular rate, although atrial contractions had ceased. At about 24 degrees C, atrial rhythm became irregular. Below 20 degrees C, atrial depolarization disappeared. Chronotropic responses to norepinephrine were suppressed at decreased temperatures, not only with respect to maximum PP shortening but also to the threshold dose for inducing sinus acceleration. Overdrive suppression was not influenced significantly by decreasing temperature. These results indicate that a temperature decrease causes suppression of SA nodal pacemaker activity, although the SA node continues to function regularly until about 25 degrees C.
利用离体、血液灌流心房标本，在9个标本中研究了温度对窦房结起搏点活动的影响。随着温度升高，PP间期缩短。在约26℃以上可维持规则的窦性心律和心房收缩。在26℃以下，尽管心房收缩已停止，但窦性去极化仍显示规则的速率。在约24℃时，心房节律变得不规则。在20℃以下，心房去极化消失。在温度降低时，对去甲肾上腺素的变时反应受到抑制，不仅在最大PP缩短方面，而且在诱导窦性加速的阈剂量方面。超速抑制不受温度降低的显著影响。这些结果表明，温度降低会导致窦房结起搏点活动受到抑制，尽管窦房结在约25℃之前仍能正常发挥功能。
