论文部分内容阅读
利用培养乳鼠心肌细胞，复制缺血再灌注损伤模型，通过观察细胞三磷酸腺苷（ＡＴＰ）、细胞内钙离子（［Ｃａ２＋］ｉ）、脂质过氧化物（ＬＰＯ）、乳酸脱氢酶（ＬＤＨ）及心肌细胞扫描电镜变化，发现：①缺血３ｈ培养液中ＬＤＨ及［Ｃａ２＋］ｉ、ＬＰＯ轻度上升，ＡＴＰ耗竭明显，细胞严重水肿；②再灌注早期ＬＤＨ、［Ｃａ２＋］ｉ及ＬＰＯ急剧增加，ＡＴＰ含量逐渐升高，再灌注１ｈ细胞水肿减轻。结果提示：①在常温、缺氧、缺糖及限制培养液量的条件下培养乳鼠心肌细胞３ｈ，再在基础培养液（ＭＥＭ）存在下培养１ｈ，能成功复制缺血再灌注损伤模型；②证实了心肌细胞缺血再灌注损伤可能与氧自由基（ＯＦＲ）作用及［Ｃａ２＋］ｉ超负荷有关。
The model of ischemia-reperfusion injury was reproduced by culturing neonatal rat cardiomyocytes. The effects of ATP, Ca2 +, LPO, LDH, And myocardial cell scanning electron microscopy showed that: ① LDH and [Ca2 +] i, LPO slightly increased in 3h ischemia, ATP depletion was obvious, severe cell edema; ② LDH, [Ca2 +] i and LPO sharply increased in early reperfusion , ATP content gradually increased, reperfusion 1h edema eased. The results suggest that: (1) Cardiomyocytes were cultured in normal temperature, hypoxia, hypoglycemic and limited culture medium for 3 h, and cultured for 1 h in the presence of basal medium (MEM) to successfully replicate the model of ischemia / reperfusion injury. ② It was confirmed that ischemia / reperfusion injury of cardiomyocytes may be related to the effect of OFR and [Ca2 +] i overload.