前列腺素E_1预处理对异丙肾上腺素性心肌损伤的保护作用

目的　探讨前列腺素E1(PGE1)预处理对急性心肌梗塞的早期和延迟保护作用。方法　ivPGE1(2 5mg·kg-1和15 0mg·kg-1)对大鼠进行预处理 ,分别于预处理后 2 0min或 2 4hip异内肾上腺素 (80mg·kg-1)造成急性心肌梗塞 ,于ip异丙肾上腺素后 2 4h取出心脏、匀浆 ,测定其丙二醛(MDA)含量 ,谷胱甘肽过氧化物酶 (GSH Px)活性 ,总超氧化物歧化酶 (T SOD)和锰 超氧化物歧化酶 (Mn SOD)活性。结果　心肌梗塞模型组心肌MDA含量明显上升 ,GSH Px活性降低 ,T SOD和Mn SOD活性增高。与模型组比较 ,两剂量PGE1预处理后 2 0min及 2 4h的各组均明显降低梗塞心肌的MDA含量 (P <0 0 1)和T SOD、Mn SOD活性 (均P<0 0 1) ,提高GSH Px活性 (P <0 0 1)。结论　前列腺素E1预处理具有预适应性早期和延迟心肌保护作用。

Pretreatment with prostaglandin E_1 attenuates myocardial injury caused by isoproterenol

AIM To investigate whether pretreatment with prostaglandin E 1 (PGE 1) might protect myocardium against peroxidative injury in early phase and in delayed phase. METHODS Rats were pretreated with PGE 1 (25 or 150 mg·kg -1 ). Isoproterenol (ISOP)(80 mg·kg -1 ) were injected peritoneally (ip) to induce acute myocardial infarction 20 minutes (early phase) or 24 hours (delayed phase) after pretreatment. Hearts were removed punctually 24 hours after ip ISOP and were assayed for content of malonaldehyde (MDA), activity of glutathione peroxidase (GSH Px) and superoxide dismutase (SOD). RESULTS ISOP caused myocardial injury with increased MDA content and SOD activity, and decreased GSH Px activity. Pretreatment with PGE 1, at each dose and in both phase, decreased the MDA content ( P< 0 01) and SOD activity ( P< 0 01), increased GSH Px activity ( P< 0 01). CONCLUSION Preconditioning by PGE 1 pretreatment attenuates ISOP induced myocardial injury in both early and delayed phase.