In a rat model of chronic myocardial infarction, intramuscular streptomycin significantly inhibited the stretch-induced decrease in MAPD90 and reduced the occurrence of premature ventricular beats.
Does streptomycin inhibit stretch-induced electrophysiological changes and arrhythmias in chronically infarcted rat hearts?
In a rat model of chronic myocardial infarction, streptomycin inhibited stretch-induced action potential shortening and reduced premature ventricular beats, suggesting a role for stretch-activated ion channels in mechanoelectric feedback.
Absolute Event Rate: 61.87% vs 57.47%
p-value: p=<0.05
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.
Cao et al. (Sun,) conducted a other in Chronic myocardial infarction (n=60). Streptomycin vs. Control (no streptomycin) was evaluated on 90% monophasic action potential duration (MAPD90) during stretching in MI hearts (ms) (p=<0.05). In a rat model of chronic myocardial infarction, intramuscular streptomycin significantly inhibited the stretch-induced decrease in MAPD90 and reduced the occurrence of premature ventricular beats.
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