Silverman N A, DuBrow I, Kohler J, Levitsky S
J Surg Res. 1984 Mar;36(3):198-204. doi: 10.1016/0022-4804(84)90088-x.
Atrioventricular-nodal-conduction abnormalities following cardiac surgery have been attributed to the potassium ion in cardioplegic solutions. To clarify the etiology of these rhythm problems, 15 dogs were subjected to (I) 60 min 4 degrees C potassium cardioplegic arrest; (II) 30 min normothermic ischemic arrest; or (III) cardiac hypothermia without ischemia. In sinus rhythm and during atrial pacing, A-H and H-V intervals, Wenckebach cycle length (WCL), atrial- and AV-nodal refractory periods (ARP and NRP) were measured at 37 degrees C before and 30 min after arrest (groups I and II) and at various myocardial temperatures (group III). Following cardioplegic arrest and reperfusion, all AV-nodal-conduction properties were unchanged from preischemic values. In contrast, unprotected ischemia significantly prolonged AV-nodal-conduction time (P less than 0.01) and myocardial hypothermia resulted in prolonged WCL (P less than 0.01), prolonged functional NRP (P less than 0.05), in addition to delayed A-H interval (P less than 0.05). The data suggest that properties of AV-nodal conduction are preserved following potassium cardioplegic arrest, but impaired by ischemic injury or persistent local cardiac hypothermia.
心脏手术后的房室结传导异常一直被归因于心停搏液中的钾离子。为了阐明这些节律问题的病因，对15只狗进行了以下实验：（I）60分钟4℃钾心停搏；（II）30分钟常温缺血停搏；或（III）无缺血的心脏低温。在窦性心律和心房起搏期间，于停搏前和停搏后30分钟（I组和II组）在37℃以及在不同心肌温度下（III组）测量A-H和H-V间期、文氏周期长度（WCL）、心房和房室结不应期（ARP和NRP）。在钾心停搏和再灌注后，所有房室结传导特性与缺血前值相比均未改变。相比之下，未保护的缺血显著延长了房室结传导时间（P<0.01），心肌低温导致WCL延长（P<0.01）、功能性NRP延长（P<0.05），此外还导致A-H间期延迟（P<0.05）。数据表明，钾心停搏后房室结传导特性得以保留，但会因缺血损伤或持续性局部心脏低温而受损。
