AIM: To study effects of anthopleurin-Q (AP-Q) on myocardial hypertrophy in rats and isolated atria in guineapigs. METHODS: Two myocardial hypertrophy models in rats were established, one introduced by levothyroxine,the other by stenosis of abdominal aorta. Cardiac myocytes morphometry and functional experiments were em-ployed to investigate effects of AP-Q. RESULTS: Low dose of AP-Q (1 μg-kg-1.d-1, ip) reduced morphologicchanges of myocardial hypertrophy in both rat models. While high dose of AP-Q (10 μg-kg-1.d-1, ip) did not, andcaused mild hydropic degeneration in cardiomyocytes. High concentration of AP-Q (30 nmol/L) enhanced thecontractility, raised automaticity, and prolonged the functional refractory period (FRP) in isolated left atria of guineapigs; higher concentration (100 nmol/L) triggered arrhythmia in right atria; low concentration of AP-Q (1 nmol/L)did not affect any myocardial properties above. CONCLUSION: Low dose of AP-Q without inotropic effect canhinder the experimental myocardial hypertrophy in rats; high dose with positive inotropic effect may be responsiblefor its toxic reaction.%目的:研究海葵素(AP-Q)对大鼠心肌肥厚及离体豚鼠心房的作用.方法:分别以甲状腺素(L-Thy)及腹主动脉狭窄建立两种大鼠心肌肥厚模型;用形态学及功能性实验研究AP-Q作用.结果:1)低剂量AP-Q(1 μg.kg-1.d-1)可改善两种肥厚模型心肌形态学变化;高剂量AP-Q(10 μg.kg-1.d-1)不能减轻L-Thy引起的心肌肥厚,且使心肌细胞轻度水变性.2)高浓度AP-Q(30 nmol/L)增强豚鼠心房收缩力,延长功能性不应期,升高自律性;更高浓度(100nmol/L)引起右心房心律失常;低浓度AP-Q(1 nmol/L)对上述心肌特性无影响.结论:不影响心肌特性的低剂量AP-Q能抑制实验性大鼠心肌肥厚;增强心收缩力的AP-Q高剂量,可能已是毒性剂量.
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