自发性高血压大鼠血管平滑肌细胞缺氧预处理的延迟保护作用

THE DELAYED PROTECTION OF HYPOXIC PRECONDITIONING ONVASCULAR SMOOTH MUSCLE CELLS OF SPONTANEOUSHYPERTENSIVE RATS SUBJECTED TO HYPOXIA/REOXYGENATION

目的：观察缺氧预处理（ＰＣ）对于自发性高血压大鼠（ＳＨＲ）血管平滑肌细胞（ＶＳＭＣ）缺氧复氧（Ｈ／Ｒ）损伤的延迟保护作用，并探讨其可能机制。方法：对ＶＳＭＣ于缺氧ＰＣ２４ｈ后进行Ｈ（２ｈ）／Ｒ（１ｈ），结束实验时测定其Ｈ／Ｒ后细胞存活率、乳酸脱氢酶（ＬＤＨ）释放和ＡＴＰ含量，并测定其金属硫蛋白（ＭＴ）量。结果：缺氧ＰＣ明显减轻Ｈ／Ｒ造成的ＳＨＲ的ＶＳＭＣ存活率下降、ＡＴＰ耗竭和ＬＤＨ释放，并使细胞内应激蛋白ＭＴ含量升高１．３倍，上述指标与正常血压对照组ＷＫＹ大鼠ＶＳＭＣ的结果相近。结论：培养的ＳＨＲ的ＶＳＭＣ亦存在ＰＣ的延迟保护作用，其保护机制涉及ＭＴ合成增多。

Objective: To investigate the delayed protective effects of hypoxic preconditioning on vascular smooth muscle cells (VSMC) of spontaneous hypertensive rats (SHR) subjected to hypoxia/reoxygenation (H/R) injury and the protective mechanism. Methods: Hypoxic PC was performed 24 h prior to H/R injury in VSMC cultured from SHR and WKY rats, and the cell viability, lactate dehydrogenase (LDH) release and cellular ATP content after H/R were determined. Metallothionein (MT) content in VSMC was also detected. Results: Hypoxic PC decreased H/R induced cellular LDH release, ATP depletion and improved cell viability, and increased MT content in VSMC of SHR. The above effects were similar to that in VSMC of WKY rats. Conclusion: Cultured VSMC of SHR have delayed protective effect of hypoxic PC. PCinduced cellular MT increase is involved in the protective mechanism.