大鼠短暂缺血引起的微血管通透性增加对缺血后心肌功能的影响

Effects of transient myocardial ischemia-induced increase of microvascular permeability on the contractile function in rats

目的：探讨大鼠心肌短暂缺血后微血管通透性的变化在心肌缺血再灌注损伤发病机制中的作用。方法：在心肌缺血前颈外静脉注射异硫氰酸荧光素标记的白蛋白（ＦＩＴＣ－ＢＳＡ，３．０ｍｙ／ｋｇ），１ｈ后致心肌缺血再灌注，测定心肌收缩功能动态变化和心肌组织ＦＩＴＣ－ＢＳＡ浓度。结果：１５、２０ｍｉｎ心肌缺血或缺血后再灌注１ｈ可引起心肌微血管通透性明显增加。缺血组心肌ＦＩＴ－ＢＳＡ由假结扎组的（１６６．０±７．９）μｇ／ｇ心肌增加到（２４０．６±７．８）μｇ／ｇ（ＩＳ１５组）和（２６７．４±７．９）μｇ／ｇ心肌（ＩＳ２０组）（Ｐ＜０．０１）。再灌注１ｈ后，ＦＩＴＣ－ＢＳＡ减低至（２２４．８±１１．８）μｇ／ｇ心肌（ＭＳ１５组）和（２４１．７±６．０）μｇ／ｇ心肌（ＭＳ２０组），但仍比假结扎组高３５．４％和４５．６％。短暂缺血后心肌功能明显减退，再灌注后逐渐恢复，但仍未达到假结扎组水平。ＦＩＴＣ－ＢＳＡ增加越明显，心肌功能障碍越严重。结论：短暂缺血所致的微血管通透性增加可能参与了顿抑心肌的发生机制，抑制短暂缺血引起的心肌徽血管通透性增加可改善缺血后的心功能障碍。

Objective:To investigate the effect of transient ischemia-induced microvascular permeability changes in the pathogensis of myocardial ischemia and reperfusion injury. Methods: Fluorescein isothiocyanate labelled albumin(FITC- BSA 3. 0 mg/kg) was injected into external juglar vein before myocardial ischemia. After 1 h, myocardial ischemia was induced and followed by reperfusion. The dynamic changes of myocardial contractile function andconcentration of FITC-BSA in ischemic myocardium were deternuned- Results: 15 and 20 min of myocardial ischemia or ischemia followed by 1h of reperfusion could result in increase of myocardial microvascular permeability significantly. The concentrations of FITC-BSA of myocardial tissue increased from 166. 0±7.9(Sham-occlusion group)to 240. 6±7.8(IS15)and 267.4±7.9(IS20)μg/g myocardium in ischemia groups,respectively(P<0.01).After 1h of reperfusion,the concentrations were decreased reversely from ischemia groups,which were 224. 8±11. 8 (MS15) and 241. 7±6.0(MS20) μg/g myocardium,but still higher than that of sham-occlusion group by 35. 4% and 45. 6%,respectively.The myocardial contractile function after transient ischemia significantly impaired and gradually recovered after reperfusion, but not to the level of sham-occlusion group. The more significant the concentration of FITC-BSA, the more serious the myocardial stunning.Conclusion:The increase of microvascular permeability resulting from transient ischemia might be involved in the pathogenesis of stunned myocardium, and inhibition of transient ischemia-induced increase of myocardial microvascular permeability could improve the contractile dysfunction.