Glucocorticoid pretreatment protects cardiac function and induces cardiac heat shock protein 72

被引:58
作者
Valen, G [1 ]
Kawakami, T
Tähepôld, P
Dumitrescu, A
Löwbeer, C
Vaage, J
机构
[1] Karolinska Hosp, Crafoord Lab Expt Surg L6 00, S-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Thorac Surg, S-17176 Stockholm, Sweden
[3] Huddinge Univ Hosp, Dept Clin Chem, S-14186 Huddinge, Sweden
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2000年 / 279卷 / 02期
关键词
methylprednisolone; dexamethasone; hydrocortisone; ischemia-reperfusion;
D O I
10.1152/ajpheart.2000.279.2.H836
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute administration of glucocortiocoids reduces inflammation. Increasing knowledge of the mechanisms of action indicate that pretreatment with glucocorticoids could have organ-protective effects. We investigated whether pretreatment with methylprednisolone (MP) protected the heart against ischemia-reperfusion dysfunction, and we hypothetized that this protection might be due to induction of the cardioprotective heat shock protein 72 (HSP72). Rats were given vehicle or MP-40 mg/kg im as a double injection starting either 24 or 120 h (5 days) before their hearts were excised for Langendorff perfusion (n = 6-11 hearts in each group). MP improved left ventricular function and coronary flow during reperfusion after 30 min of global ischemia and reduced infarct size. Cardiac HSP72 gradually increased in a 24-h time course after MP treatment, and the increase was sustained 5 days afterward (immunoblotting). HSP72 mRNA was either reduced or unchanged, indicating a posttranscriptional regulation. Pretreatment with hydrocortisone or dexamethasone (n = 7-8 hearts of each) similarily increased cardiac HSP72 24 h afterward. This paper demonstrates that glucocorticoids increase cardiac HSP72 and protect organ function against ischemia-reperfusion injury.
引用
收藏
页码:H836 / H843
页数:8
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