摘要
目的研究中叶素(Intermedin,IMD)对大鼠心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤的保护作用及其可能机制。方法Langendorff方法灌流离体心脏,并造成I/R模型,以Power Lab多导生理记录仪记录灌流心脏心功能的变化,收集灌流后心肌组织及灌流液进行生化检测。结果IMD再灌注明显改善I/R造成的心功能抑制和组织损伤,可升高△LVP、LV±dp/dtmax,降低LVDP,增加心率及冠脉流量,同时使心肌LDH、总蛋白和肌红蛋白的漏出及心肌组织MDA生成明显减少,而心肌组织cAMP含量明显增加。且IMD的上述效应与同浓度ADM的效果相近。此外,I/R后心肌IMD受体Bmax和Kd值均增加。结论IMD有明显的抑制心脏I/R损伤的作用,该作用可能通过cAMP途径介导,且IMD抗I/R损伤的作用与强内源性心血管保护肽肾上腺髓质素相仿。
Aim To determine the protective effects of IMD on ischemia/reperfusion （I/R） injury and its possible mechanism. Method Isolated rat hearts were perfused by Lmgendorff mode, and after 45 min global ischemia and 30 min reperfusion ventricular function was measured on a Power Lab, and adequate amount of ventricular tissues and perfusate were collected for bio- chemical measurement. Results Treatment with IMD during the reperfusion period significantly attenuated the effects of I/R on cardiac function inhibition and tissue injury. increase in Compared with I/R group, IMD induced a LVP, LV（ dp/dtmax, HR and CF, where-as induced decrease in LVDP. Reperfusion with IMD exerted decrease in LDH, total protein, Mb and MDA content compared with I/R group, but increased myocardial cAMP content. All these values were similar to the effects of ADM. Furthermore, I/R induced signifi- cant increase in Bmax and Ka value. Conclusion IMD exerted beneficial effects on cardiac injury induced by I/R which might be mediated by cAMP pathway. And the cardioprotective effects of IMD were equal to ADM, a potent cytoprotective factor.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第5期592-596,共5页
Chinese Pharmacological Bulletin
基金
山西省基础研究资助项目(No2006021042)
