机械牵张加重模拟缺血缺氧心肌细胞损伤的研究

Mechanical stretch aggravates cardiomyocyte injury caused by ischemia/hypoxia

目的 验证机械牵张加重模拟缺血缺氧对心肌细胞的损伤效应。方法 利用所建立的心肌细胞体外牵张模型 ,模拟施加缺血缺氧因素 ,观察心肌细胞形态、培养液中乳酸脱氢酶 (LDH)含量及碘化丙啶 (PI)染色阳性细胞比例的变化。结果 10 %牵张后 ,心肌细胞形态完整 ,LDH及PI染色阳性细胞比例无明显变化。模拟缺血缺氧后形态明显破坏 ,LDH及PI染色阳性细胞比例显著增加。牵张复合模拟缺血缺氧后 ,细胞形态破坏加剧 ,LDH含量急剧上升 ,PI染色阳性细胞比例进一步显著增加 (P <0 .0 1)。结论 机械牵张加剧了模拟缺血缺氧对心肌细胞的损伤效应 ,提示严重烧伤早期过多过快补液导致心脏前负荷的迅速增加对心肌组织产生牵拉可能会加剧业已存在的心肌细胞损伤 ,从而进一步促进了心肌损害的发生。

Objective To clarify if mechanical stretch aggravates cardiomyocyte injury caused by ischemia/ hypoxia. Methods Cardiomyocytes were cultured in vitro and a uniaxial static mechanical stretch device was successfully manufactured. Lactate dehydrogenase (LDH) leaking, ratio of propidium iodide (PI) staining positive cells, and cardiomyocyte morphology were observed to test the effects of mechanical stretch cardiomyocytes exposed to simulated ischemia/hypoxia. Results Mechanical stretch (10%) resulted in no obvious changes of morphology of cardiomyocytes, LDH leakage and ratio of PI staining positive cells ( P >0.05). When mechanical stretch and simulated ischemia/hypoxia were imposed on cardiomyocytes simultaneously, LDH leakage and ratio of PI staining positive cells increased greatly and cell morphology changed obviously ( P <0.01). Conclusion Mechanical stretch may aggravate cardiomyocyte injury caused by ischemia/hypoxia, which may be another pathological cause of shock heart.