前列腺素介导缓激肽诱导预适应对缺血再灌心肌的保护作用(英文)

Cardioprotection of bradykinin induced preconditioning mediated by prostaglandin 1

在大鼠离体心脏观察了前列腺素介导缓激肽诱导的预适应对缺血再灌心肌的保护作用．３０ｍｉｎ缺血和３０ｍｉｎ再灌引起心功能降低（左室内压和左室内压最大上升速率下降），冠脉流量和心率降低以及肌酸激酶（ＣＰＫ）释放增加．缺血预适应（５ｍｉｎ缺血，５ｍｉｎ再灌，重复３次）能显著改善心功能，促进心率和冠脉流量的恢复，减少ＣＰＫ释放．其作用不受吲哚美辛（１０μｍｏｌ·Ｌ－１预先灌流３０ｍｉｎ）影响．预先用缓激肽（０．５μｍｏｌ·Ｌ－１）处理５ｍｉｎ产生缺血预适应样心肌保护作用，表现为促进心功能恢复，减少ＣＰＫ释放．该作用被预先灌流吲哚美辛取消．对照组，缺血再灌组，缓激肽组，吲哚美辛加缓激肽组的ＣＰＫ分别为（０．２８±０．０３），（２．２３±０．０６），（０．３９±０．０９），（１．８７±０．０５）μｍｏｌ·ｍｉｎ－１·ｇ－１湿组织．

Cardioprotection of prostaglandin mediated bradykinin (BK) induced preconditioning was studied in the isolated rat hearts. Thirty minutes of global ischemia and 30 min of reperfusion caused a decrease in left ventricular pressure (LVP), the maximal rate of rise of ventricular pressure (+dp/dt max ), coronary flow (CF) and heart rate (HR) and an increased release of creatine phosphate kinase (CPK). Preconditioning induced by 3 cycles of 5 min ischemia and 5 min reperfusion improved LVP, +dp/dt max , CF and HR and reduced CPK release. The protection of preconditioning was not affected by exposure to indometacin (Indo, 10 μmol·L 1 ) for 30 min prior to preconditioning. Pretreatment with BK (0.5 μmol·L 1 ) for 5 min also induced the same protection as ischemic preconditioning, as assessed by the improved cardiac function and the reduced CPK release. However, the effects of BK were abolished by Indo. CPK was (0.28±0.03),(2.23±0.06),(0.39±0.09) and (1.87±0.05) μmol·min 1 ·g 1 wet weight for control, ischemia reperfusion, BK and Indo+BK, respectively. These results suggest that the cardioprotection of BK induced preconditioning be due to stimulation of prostaglandin production.