摘要
目的：研究不同缺血时间对培养窦房结细胞Ｇｌｖｃｏｇｅｎ，ＳＤＨ，ＬＤＨ和ＡＮＦ的损伤及卡托普利对这种损伤的保护作用。材料和方法：取２００只新生４天ＳＤ乳鼠的心窦房结组织用于细胞培养，再制作拟缺血模型，然后采用下列方法进行实验：ＰＡＳ反应示精原颗粒，Ｐｅａｒｓｏｎ法示琥珀酸脱氢酶（Ｓｕｃｃｉｎａｔｅ ｄｅｈｙｄｒｏｇｅｎａｓｅ，ＳＤＨ），Ｐｒｅｓｔｏｎ法示乳酸脱氢酶（Ｌａｃｔａｔｅ ｄｅｈｙｄｒｏｇｅｎａｓｅ， ＬＤＨ），免疫细胞化学方法（ＡＢＣ法）示心钻素（Ａｔｒｉａｌ ｎａｔｒｉｕｒｅｔｉｃ ｆａｃｔｏｒ，ＡＮＦ），并对实验结果作图像分析。结果：缺血６０’时，培养细胞的ＬＤＨ，ＳＤＨ和ＡＮＦ活性明显受损，糖原颗粒也明显减少；缺血 ９０’时，这种缺血损伤进一步发展，糖原颗粒几乎耗竭；而缺血 ９０’＋Ｃａｐｔｏｐｒｉｌ处理组的缺血损伤明显减轻（与缺血组相比 Ｐ＜０．０５）。结论；从形态学上观察到，卡托普利对新生 ＳＤ乳鼠窦房结培养细胞的细胞器和膜性结构及细胞功能的缺血损伤有明显保护作用。
Objective: To investigate the effects of prolonged ischemia on the activities and the volume of glycogen, SDH, LDH and ANF in the cultured sinuatrial nale (SAN) cells and the protective effects of captopril on the ischemic injury. Material and Methods: 200 newborn SD rats (4- daysold ) were used. The methods included cell culture, ischemic model, PAS, Preston's and Pearson's reactions, immunocytochemical reaction (ABC) and image analysis for separately demonstrating the volume and activities of glycogen, SDH, LDH and ANF in cultured cells of SAN. Results: The results showed that the activities of LDH, SDH and ANF in cultured SAN cells were all obviously injured at 60 min following the ischemia. At the same time, the granules of glycogen were also obviously reduced. The ischemic injuries became more serious with the pro- longed ischemia and the granules of glycogen were almost exhausted at 90 min following the is- chemia. The ischemic injuries in the group with captopril were found to be significant light (P< 0. 05) compared with the ischemic group. Conclusion: Our study suggests that captopril has ob- viously protective effects on the structure and the function of the cultured SAN cells of the newborn SD rats.
出处
《解剖学杂志》
CAS
CSCD
北大核心
1999年第5期427-432,共6页
Chinese Journal of Anatomy
关键词
窦房结
缺血损伤
卡托普利
sinuatrial node
ischemic injury
captopril
