论文部分内容阅读
目的 :观察通过短时结扎在体豚鼠升主动脉致其左心室后负荷增加时是否会引起机械电反馈 ,并观察这种效应是否能够被链霉素抑制。据此来评价牵张激活的离子通道 (stretch activatedchannels ,SACs)是否参与了机械电反馈活动。方法 :采用单相动作电位记录技术 ,记录在体豚鼠左心室前中壁的单相动作电位的过程中结扎其升主动脉 5s ,间隔 5min重复 1次 ,在重复之前由颈静脉注射链霉素 (2 0mg/kg) ,测量 5 0 %和 90 %单相动作电位复极时程 (APD50 和APD90 )并计算结扎升主动脉诱发心律失常的发生率。结果 :应用链霉素前 ,短时结扎升主动脉使左心室后负荷由 (30± 8)mmHg(1mmHg =0 .133kPa)增加到 (70± 17)mmHg(P <0 .0 5 ) ,伴随后负荷的增加 ,APD5 0由 (78± 13)ms缩短为 (6 0± 14 )ms(P <0 .0 5 ) ,APD90 由 (119± 18)ms缩短为 (110± 19)ms(P<0 .0 5 ) ,并且可以观察到 6 7%的心脏发生牵张诱发的心律失常 ;应用链霉素后 ,短时结扎升主动脉可引起左心室后负荷相似的变化 ,但APD50 和APD90 未发生明显改变 ,且只有 17%的心脏发生心律失常。结论 :增加左心室后负荷可引起在体豚鼠心肌APD50 和APD90 缩短 ,并且可诱发心律失常。链霉素对此均有抑制作用 ,提示SACs可能参与了该过程。
OBJECTIVE: To observe whether mechanical feedback could be induced by short-term ligation after increased load of left ventricle in the ascending aorta of guinea pigs and to observe whether this effect can be inhibited by streptomycin. Based on this, we evaluated if stretch activatedchannels (SACs) are involved in the mechano-electric feedback. Methods: Monophasic action potential recording technique was used to record the ascending aorta in the anterior wall of the left ventricle of guinea pigs. The ascending aorta was ligated for 5 seconds and repeated 5 minutes. The streptomycin (20 mg / kg). The repolarization duration (APD50 and APD90) of 50% and 90% single-phase action potentials were measured and the incidence of arrhythmia induced by ligation of the ascending aorta was calculated. RESULTS: Before and after streptomycin administration, the left ventricular posterior load was increased from (30 ± 8) mmHg (1mmHg = 0.133kPa) to (70 ± 17) mmHg (P <0.05) APD50 was shortened from (78 ± 13) ms to (60 ± 14) ms (P <0. 05) with APD90 shortened from (119 ± 18) ms to (110 ± 19) ms P <0.05), and 67% cardiac arrhythmia induced by cardiac distraction was observed. Short-term ligation of the ascending aorta with streptomycin caused similar changes in left ventricular afterload, but APD50 and APD90 did not change significantly, and only 17% of cardiac arrhythmias occur. CONCLUSION: Increasing left ventricular afterload can cause shortening of APD50 and APD90 in guinea pig myocardium and inducing arrhythmia. Streptomycin inhibited this, suggesting that SACs may be involved in the process.