心脏纤维化大鼠心室颤动

S. Marak, A. de Jongh
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引用次数: 0

摘要

先前的研究表明,在慢性心力衰竭患者中,血管紧张素II (Ang II)的使用会导致大鼠心房和心室纤维化。我们假设纤维化产生一种促进心室颤动(VF)诱导的底物。研究对象是十四、八周龄的Sprague-Dawley大鼠。11例接受植入微型泵的Ang II (9 /spl mu/g/hr)治疗4周。治疗后,打开胸腔,以三倍于起搏阈值的强度对心房和心室施加50hz刺激,时间分别为2.5、5和10 s。VF在治疗组(11 / 6)诱导率高于未治疗组(3 / 0,P < 0.05)。12个VF发作中有3个在刺激结束后持续(>0 s),而其余的VF发作在刺激结束后不持续(bbb30 ms和< 10 s)。我们的研究结果表明,Ang II治疗诱导的心脏纤维化为持续的VF创造了一个底物。
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Ventricular fibrillation in rats with cardiac fibrosis
Previous studies have shown that administration of angiotensin II (Ang II) 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 Ang II (9 /spl mu/g/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 Ang II treatment creates a substrate for sustained VF.
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