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Ventricular fibrillation in rats with cardiac fibrosis

机译:心肌纤维化大鼠的心室颤动

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Previous studies have shown that administration of angiotensin II (AngII) causes atrial and ventricular fibrosis in rats, as is found in patients with chronic heart failure. We hypothesize that fibrosis creates a substrate that promotes the induction of ventricular fibrillation (VF). Fourteen, eight-week old, Sprague-Dawley rats were studied. Eleven received a four-week treatment of AngII (9 μg/hr) from an implanted mini-pump. After treatment, the chest was opened, and 50 Hz stimulation at a strength of three times the pacing threshold was applied across the atria and ventricles for 2.5, 5, and 10 s. VF was more inducible in treated rats (6 of 11) than untreated rats (0 of 3, P<0.05). Three of 12 VF episodes were sustained (>10 s) while the remaining VF episodes were nonsustained (>30 ms and <10 s) after stimulation ended. Our results suggest that cardiac fibrosis induced by AngII treatment creates a substrate for sustained VF.
机译:先前的研究表明,血管紧张素II(Angii)的给药导致大鼠心房和心室纤维化,如慢性心力衰竭患者所发现的。我们假设纤维化产生促进心室纤维化诱导(VF)的底物。研究了四周,八周,Sprague-Dawley大鼠。 11,从植入的迷你泵接受了4周的血管(9μg/ hr)的治疗。治疗后,胸部打开,搏动阈值的强度为50Hz刺激,在ATRIA和脑室中施加2.5,5和10 s。 VF在治疗的大鼠(6个中的6个)比未处理的大鼠(0 of 3,P <0.05)中更诱导。在刺激结束后,持续(> 10秒)持续(> 10秒)中的三种(> 10秒),而剩余的VF发作是被抑制的(> 30ms和<10秒)。我们的研究结果表明,Angii治疗诱导的心肌纤维化会产生持续VF的底物。

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