Smith P K, Buhrman W C, Ferguson T B, Levett J M, Cox J L
Circulation. 1983 Sep;68(3 Pt 2):II41-8.
Atrioventricular conduction abnormalities have become more frequent since the reintroduction of cardioplegic techniques for myocardial preservation during cardiac surgery. An animal model was developed to clarify the role of atrial septal hypothermia in the preservation of the primary site of postoperative conduction delay, the AV node. In our study, 10 animals served as the control group. They were subjected to 40 min of cardioplegic arrest during which the heart was protected with multidose cold potassium cardioplegia. Atrial septal temperatures averaged 27.4 degrees +/- 1.2 degrees C during cardioplegic arrest. We treated 10 additional animals (study group) similarly, except that atrial hypothermia was augmented by intracavitary or specialized topical techniques, which resulted in an average atrial septal temperature of 20.8 degrees +/- 3.3 degrees C (p less than .05). Detailed electrophysiologic studies of both groups were performed at 37 degrees C before and after cardioplegic arrest. Significant prolongation of AV nodal, and to a lesser extent His-Purkinje, conduction times was noted in the control group, but no conduction abnormalities occurred in the study group receiving augmented atrial hypothermia. Thus, conduction block in the specialized conduction system after cardioplegic arrest appears to be related to the adequacy of hypothermic preservation of the atrial septum and can be prevented by augmented atrial hypothermia.
自从在心脏手术中重新引入用于心肌保护的心脏停搏技术以来，房室传导异常变得更加频繁。我们建立了一个动物模型，以阐明房间隔低温在保护术后传导延迟的主要部位——房室结方面的作用。在我们的研究中，10只动物作为对照组。它们经历了40分钟的心脏停搏，在此期间心脏用多剂量冷钾心脏停搏液进行保护。心脏停搏期间房间隔温度平均为27.4摄氏度±1.2摄氏度。我们对另外10只动物（研究组）进行了类似的处理，只是通过腔内或特殊局部技术增强了心房低温，这使得房间隔平均温度为20.8摄氏度±3.3摄氏度（p<0.05）。在心脏停搏前后，对两组动物在37摄氏度下进行了详细的电生理研究。对照组中观察到房室结传导时间显著延长，希氏-浦肯野系统传导时间延长程度较小，但在接受增强心房低温的研究组中未出现传导异常。因此，心脏停搏后特殊传导系统中的传导阻滞似乎与房间隔低温保存的充分性有关，并且可以通过增强心房低温来预防。
