Lipasti J A, Nevalainen T J, Alanen K A
Basic Res Cardiol. 1982 Jul-Aug;77(4):404-10. doi: 10.1007/BF02005340.
The relationship between ischemic contracture and no-reflow phenomenon was studied in 59 isolated rat hearts during global ischemia. The contracture was measured by a water-filled balloon catheter placed in the left ventricular lumen. The time of onset of contracture was changed by preischemic infusion with buffer containing 0.5 mmoles/l iodoacetate (IAA) in order to get early contracture, and by hypothermia which delayed the development of contracture. The first signs of contracture were noticed in normothermia (37 degrees C) at 11 minutes, in hypothermia (26 degrees C) at 25 minutes, and in the IAA-infused group at 3 minutes. The completion of contracture occurred in these groups at 25, 90 and 11 minutes, respectively. The myocardial perfusability was tested at the pre- and postcontracture state by infusing 0.1% fluorescein in isotonic saline into the cannulated aortic root. The myocardial area perfused with fluorescein was quantified in colour photographs taken under ultraviolet light of frozen whole-heart sections. The myocardial perfusion - expressed ad percent of myocardial area - was 99% at the precontracture state in normothermia, 95% in hypothermia and 100% in the IAA-infused group. At the postcontracture state, the myocardial perfusion in these groups was 80, 56 and 18%, respectively. It was concluded that the no-reflow phenomenon in isolated rat heart is closely associated with the development of myocardial contracture during global ischemia.
在59个离体大鼠心脏的全心缺血过程中，研究了缺血性挛缩与无复流现象之间的关系。通过置于左心室腔的充水球囊导管测量挛缩情况。为了引发早期挛缩，在缺血前输注含0.5毫摩尔/升碘乙酸（IAA）的缓冲液来改变挛缩的起始时间，通过低温来延迟挛缩的发展。挛缩的最初迹象在正常体温（37摄氏度）下11分钟时出现，在低温（26摄氏度）下25分钟时出现，在IAA输注组3分钟时出现。这些组中挛缩分别在25、90和11分钟时完成。在挛缩前和挛缩后状态，通过向插管的主动脉根部输注等渗盐水中的0.1%荧光素来测试心肌灌注性。在冷冻的全心切片的紫外光下拍摄的彩色照片中对灌注有荧光素的心肌面积进行定量。以心肌面积百分比表示的心肌灌注在正常体温下挛缩前状态为99%，低温下为95%，IAA输注组为100%。在挛缩后状态，这些组中的心肌灌注分别为80%、56%和18%。得出的结论是，离体大鼠心脏中的无复流现象与全心缺血期间心肌挛缩的发展密切相关。
