摘要
目的观察葱白提取物(FOB)对缺血再灌注(I/R)心功能及细胞内游离Ca2+的影响,探讨FOB对I/R损伤的保护及其可能机制。方法利用Langendorff系统建立大鼠I/R心脏模型并观察心功能变化;采用激光扫描共聚焦显微镜,借用Fluo-3/AM荧光染色技术观察心肌细胞内Ca2+强度。结果FOB能明显保护I/R造成的心肌损伤,并呈剂量依赖性。随着FOB剂量增加,心脏左室发展压、左室舒张末压、左室最大收缩速率、冠脉血流量都逐渐增加,左室最大舒张速率逐渐减少;心脏痉挛度逐渐减弱,心律失常的发生越来越少。FOB可使I/R后心肌细胞内Ca2+荧光强度明显减少,并随浓度增高。结论FOB可显著改善I/R心肌的舒缩功能,其机制可能是FOB减轻I/R心肌细胞内游离钙浓度的增加。
Objective To ohserve the effects of fistular onion hulh extract(FOB)on ischemia - reperfusion(I/R) injury and intracellular free Ca^2+ increase,which further clarify the protection and mechanism of FOB on I/R injury in rat hearts in vitro. Methods The heart models of I/R in vitro in rats were setup through using Langendorff - perfusion system. The fluorescence intensity of intracellular Ca^2+ in cardiomyocytes of rats was detected with Flup - 3/AM loading by the laser scanning confocal microscopy. Results FOB markedly antagonized I/R injury via recovery of heart functions with dose - dependent in isolated rat hearts in vitro. With increase of dose of FOB(25 g/L, 50 g/L and 100 g/L) ,FOB could significantly increase the values of the left ventricular developed pressure,left ventricular diastolic end pressure,the maximum rising rates of left ventricular pressure, coronary arterial flow, decrease the value of the maximum dropping rates of left ventrieular pressure,as soon as relaxed the magnitude of ischemia contracture and reduced the occurrence of cardiarrhythmias. FOB obviously decreased the free Ca^2+ overloading of eardiomyocytes of I/R injury. With concentration - dependent of FOB, the effects of FOB reduced Ca^2+ overloading increasingly became strong. Conclusion FOB could markedly improve the diastolic and systolic functions of injured ischemia - reperfusion hearts. It could attribute the reasons to that FOB could decrease the Ca^2+ overloading of cardiomyocytes in I/R injury.
出处
《中西医结合心脑血管病杂志》
2009年第12期1430-1432,共3页
Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
关键词
葱白提取物
缺血再灌注
细胞内游离钙离子
心脏保护
fistular onion bulb extract
ischemia- reperfusion injury
intracellular free Ca^2+~
cardiac protection