Nath S, Lynch C, Whayne J G, Haines D E
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
Circulation. 1993 Oct;88(4 Pt 1):1826-31. doi: 10.1161/01.cir.88.4.1826.
The primary mechanism of tissue injury by radiofrequency catheter ablation is presumed to be thermally mediated. However, the myocardial cellular electrophysiological effects of hyperthermia are not well characterized. We used an in vitro model of isolated guinea pig right ventricular papillary muscle to investigate the acute cellular electrophysiological effects of hyperthermia.
Excised guinea pig right ventricular papillary muscles were pinned in a high-flow tissue bath and superfused with Tyrode's solution at 37.0 +/- 0.5 degrees C. The superfusate temperature was rapidly changed to 38.0 to 56.0 degrees C for 60 seconds and then returned to 37.0 degrees C. Conventional microelectrodes were used to measure membrane potential (Vm), maximum rate of rise of the action potential (dV/dtmax), and action potential (AP) amplitude and AP duration at 50% (APD50) and 90% (APD90) repolarization. Hyperthermia resulted in (1) a progressive depolarization of Vm at temperatures > or = 40.0 degrees C, which became more prominent at temperatures > or = 45.0 degrees C; (2) changes in the AP characterized by a temperature-dependent increase in dV/dtmax and a temperature-dependent decrease in AP amplitude, APD50, and APD90; (3) reversible loss of cellular excitability within a temperature range of 42.7 to 51.3 degrees C (median, 48.0 degrees C); (4) irreversible loss of cellular excitability and tissue injury at temperatures > or = 50.0 degrees C; and (5) the development of abnormal automaticity at temperatures > 45.0 degrees C.
Hyperthermia causes significant changes in myocardial cellular electrophysiological properties that include membrane depolarization, reversible and irreversible loss of excitability, and abnormal automaticity. There appear to be specific temperature ranges for reversible and irreversible electrophysiological changes. These observations may have important implications for tissue temperature monitoring during radiofrequency catheter ablation.
射频导管消融导致组织损伤的主要机制被认为是热介导的。然而，高温对心肌细胞电生理的影响尚未得到充分表征。我们使用离体豚鼠右心室乳头肌的体外模型来研究高温的急性细胞电生理效应。
将切除的豚鼠右心室乳头肌固定在高流量组织浴中，在37.0±0.5℃用台氏液灌注。将灌注液温度迅速升至38.0至56.0℃并维持60秒，然后恢复至37.0℃。使用传统微电极测量膜电位（Vm）、动作电位最大上升速率（dV/dtmax）、动作电位（AP）幅度以及复极化50%（APD50）和90%（APD90）时的动作电位时程。高温导致：（1）温度≥40.0℃时Vm逐渐去极化，在温度≥45.0℃时更明显；（2）动作电位变化表现为dV/dtmax随温度升高而增加，AP幅度、APD50和APD90随温度升高而降低；（3）在42.7至51.3℃（中位数48.0℃）温度范围内细胞兴奋性可逆丧失；（4）温度≥50.0℃时细胞兴奋性不可逆丧失和组织损伤；（5）温度＞4s5.0℃时出现异常自律性。
高温导致心肌细胞电生理特性发生显著变化，包括膜去极化、兴奋性的可逆和不可逆丧失以及异常自律性。可逆和不可逆电生理变化似乎存在特定温度范围。这些观察结果可能对射频导管消融期间的组织温度监测具有重要意义。
