Humphrey S M, Thomson R W, Gavin J B
J Mol Cell Cardiol. 1984 Oct;16(10):915-29. doi: 10.1016/s0022-2828(84)80028-0.
Eighty isolated rat heart preparations were used to study relationships among creatine kinase (CK) release, the loss of vascular competence (no-reflow), and the distribution of morphological changes across the left ventricular wall which occur during 60 min global ischaemia or anoxia and following subsequent oxygenated reperfusion. Hearts were either fixed with glutaraldehyde for light and electron microscopy or were injected with 1% fluorescein to define the distribution of perfusable vessels. The extent of no-reflow in half of the hearts was reduced experimentally by maintaining the diastolic volume of the left ventricular lumen during ischaemia and anoxia with a water-filled balloon. The amount of CK released during 20 min of reoxygenation or reperfusion was inversely proportional to the extent of the no-reflow area observed just prior to reoxygeneration, and also reflected the transmural extent and the severity of myocardial cell damage. Extensive contraction band necrosis was only observed in reperfused regions of anoxic hearts. In isovolumic hearts reoxygenation caused no-reflow to develop in the ventricular myocardium, and this appeared to be associated with hypercontraction. Thus the no-reflow phenomenon has a profound effect on the transmural distribution of myocardial cell damage and enzyme release which follows post ischaemic reperfusion and post anoxic reoxygenation.
80个离体大鼠心脏标本用于研究肌酸激酶（CK）释放、血管功能丧失（无复流）以及在60分钟全心缺血或缺氧期间及随后氧合再灌注后左心室壁形态学变化分布之间的关系。心脏要么用戊二醛固定用于光镜和电镜检查，要么注射1%荧光素以确定可灌注血管的分布。通过在缺血和缺氧期间用水囊维持左心室腔的舒张容积，实验性地减少了一半心脏的无复流程度。在复氧或再灌注20分钟期间释放的CK量与再氧合前观察到的无复流区域范围成反比，并且还反映了透壁范围和心肌细胞损伤的严重程度。广泛的收缩带坏死仅在缺氧心脏的再灌注区域观察到。在等容心脏中，复氧导致心室心肌出现无复流，这似乎与过度收缩有关。因此，无复流现象对缺血后再灌注和缺氧后复氧后心肌细胞损伤和酶释放的透壁分布有深远影响。
