Miyamae S
Department of Physiology, Kanazawa Medical University, Ishikawa, Japan.
J Electrocardiol. 1992 Jan;25(1):45-51. doi: 10.1016/0022-0736(92)90129-n.
Using standard microelectrode techniques, the effects of strontium (Sr++) ions on action potential (AP) repolarizations in rabbit sinoatrial node (SAN) cells were studied. In a nominally magnesium-free, calcium-free solution, Sr++ (0.5-3.55 mmol) produced an early afterdepolarization (EAD) and a prolongation of the AP. Until now, no experimental evidence has been presented in favor of an EAD mechanism in SAN cells. Superfusion of the SAN cells with 0.5 mmol Sr++ solution containing 1-5 mmol magnesium (Mg++) or 0.5 mmol calcium (Ca++) did not induce the EAD. Increasing the extracellular Mg++ to 1-5 mmol did not affect the EAD induced by superfusion with 3.55 mmol Sr++ solution. Increasing the extracellular Ca++ to 0.5 mmol suppressed the 3.55 mmol Sr(++)-induced EAD. The presence of 0.3 mmol manganese (Mn++) suppressed the EAD induced by superfusion with 0.5 mmol Sr++ solution. The EAD did not occur in the presence of 1 x 10(-6) mol nitrendipine or 2 x 10(-6) mol diltiazem hydrochloride. The presence of 0.03 mmol Mn++ did not significantly alter the 0.5 mmol Sr(++)-induced EAD. These results suggest that a slow inward Sr++ current through the Ca++ channel has an important role in the development of the EAD.
采用标准微电极技术,研究了锶(Sr++)离子对兔窦房结(SAN)细胞动作电位(AP)复极化的影响。在名义上无镁、无钙的溶液中,Sr++(0.5 - 3.55 mmol)产生早期后去极化(EAD)并延长动作电位。到目前为止,尚无实验证据支持窦房结细胞中存在EAD机制。用含1 - 5 mmol镁(Mg++)或0.5 mmol钙(Ca++)的0.5 mmol Sr++溶液对窦房结细胞进行灌流未诱发EAD。将细胞外Mg++增加到1 - 5 mmol并不影响用3.55 mmol Sr++溶液灌流诱发的EAD。将细胞外Ca++增加到0.5 mmol可抑制3.55 mmol Sr(++)诱发的EAD。存在0.3 mmol锰(Mn++)可抑制用0.5 mmol Sr++溶液灌流诱发的EAD。在存在1×10(-6) mol尼群地平或2×10(-6) mol盐酸地尔硫䓬时未出现EAD。存在0.03 mmol Mn++并未显著改变0.5 mmol Sr(++)诱发的EAD。这些结果表明,通过钙通道的缓慢内向Sr++电流在EAD的发生中起重要作用。