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Abstract: Objective: To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin (SM) on these changes in vivo. Methods: Sixty Wistar rats were divided randomly into four groups: a control group (n=15), an SM group (n=15), a myocardial infarction (MI) group (n=15), and an MI+SM group (n=15). Chronic MI was obtained by ligating the left anterior descending branch (LAD) of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels (SACs) was achieved by intramuscular injection of SM (180 mg/(kg∙d)) for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential (MAP). The effect of stretching was examined by assessing the 90% monophasic action potential duration (MAPD₉₀), premature ventricular beats (PVBs), and ventricular tachycardia (VT). Results: The MAPD₉₀ decreased during stretching in both the control (from (50.27±5.61) ms to (46.27±4.51) ms, P<0.05) and MI groups (from (65.47±6.38) ms to (57.47±5.76 ms), P<0.01). SM inhibited the decrease in MAPD₉₀ during inflation ((46.27±4.51) ms vs. (49.53±3.52) ms, P<0.05 in normal hearts; (57.47±5.76) ms vs. (61.87±5.33) ms, P<0.05 in MI hearts). The occurrence of PVBs and VT in the MI group increased compared with that in the control group (PVB: 7.93±1.66 vs. 1.80±0.86, P<0.01; VT: 7 vs. 1, P<0.05). SM decreased the occurrence of PVBs in both normal and MI hearts (0.93±0.59 vs. 1.80±0.86 in normal hearts, P<0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P<0.01). Conclusions: Stretch-induced MAPD₉₀ changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback (MEF), but that there might be other mechanisms involved in causing VT in chronic MI.

链霉素抑制慢性心肌梗死大鼠心脏牵张时的电生理改变

研究目的：以往研究发现链霉素作为牵张激活离子通道阻断剂，可抑制机械电反馈时心脏的电生理效应，但多为离体研究。由于慢性心肌梗死时心肌细胞间存在较为明确的牵拉，故本研究探讨了在大鼠体内应用链霉素是否可以抑制慢性心肌梗死大鼠心脏牵张诱导的电生理改变。
创新要点：首次探讨了在大鼠体内应用链霉素对慢性心梗时心脏机械电反馈现象的影响。
研究方法：60只Wistar大鼠随机分为4组：对照组（n=15）、链霉素组（n=15）、心梗组（n=15）和心梗＋链霉素组（n=15）。结扎左前降支（LAD）8周制备慢性心梗模型，术后肌注链霉素（180 mg/(kg∙d)）7天后，钳夹主动脉5秒牵张心脏，观察牵张效应包括90%单相动作电位时程（MAPD₉₀）、室性期前收缩（PVB）、室性心动过速（VT）等。
重要结论：研究结果发现牵张使得对照组（(50.27±5.61) ms vs. (46.27±4.51) ms, P<0.05）和心梗组（(65.47±6.38) ms vs. (57.47±5.76) ms, P<0.01）大鼠心脏MAPD90缩短。链霉素可抑制牵张引起的正常（(46.27±4.51) ms vs. (49.53±3.52) ms, P<0.05）和梗死心肌（(57.47±5.76) ms vs. (61.87±5.33) ms, P<0.05）MAPD90的缩短（见图1）。牵张后心梗组大鼠心肌PVB（7.93±1.66 vs. 1.80±0.86, P<0.01）和VT（7 vs. 1, P<0.05）的发生较对照组增多。链霉素可抑制正常（0.93±0.59 vs. 1.80±0.86, P<0.05）和梗死心肌（5.40±1.18 vs. 7.93±1.66, P<0.01）PVB的发生。以上结果表明，牵张诱导慢性梗死心肌出现MAPD₉₀的改变并产生心律失常。在大鼠体内应用链霉素可降低PVB的发生但对VT无影响。因此，牵张激活离子通道可能参与到慢性心梗的机械电反馈中，同时可能有其他机制参与到牵张诱导的VT中。

关键词：心律失常；机械电反馈；单相动作电位；心肌梗死；链霉素

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