Humphrey S M, Gavin J B
Pathology. 1985 Jul;17(3):437-42. doi: 10.3109/00313028509105497.
Changes in the contracture and stiffness of ventricular walls during ischemia and their effect on vascular reperfusion were studied in isolated rat hearts. Global ischemia was induced by stopping the flow of oxygenated perfusate for 60 min. Contracture pressures generated against water-filled left ventricular balloons maintained at diastolic volume increased between 8 and 25 min of ischemia and declined thereafter. On the other hand, left ventricular wall stiffness, estimated from the pressure required to periodically inflate otherwise uninflated balloons to diastolic volume, increased rapidly between 20 and 30 min of ischemia, and more slowly thereafter. Inflation of balloons following 30 or more min of ischemia caused significant reductions in left ventricular wall stiffness. Similar brief inflation after 60 min of ischemia allowed aqueous sodium fluorescein to perfuse the subendocardial half of the left ventricular wall which was otherwise not accessible to reperfusion. This reversal of the no reflow phenomenon was accompanied by a reduction in myocardial wall stiffness, stretching of myocytes and increased patency of myocardial capillaries.
在离体大鼠心脏中研究了缺血期间心室壁挛缩和僵硬度的变化及其对血管再灌注的影响。通过停止含氧灌注液流动60分钟诱导全心缺血。在缺血8至25分钟期间，对抗维持在舒张容积的充水左心室球囊产生的挛缩压力增加，此后下降。另一方面，根据将原本未充气的球囊周期性充气至舒张容积所需的压力估算的左心室壁僵硬度，在缺血20至30分钟之间迅速增加，此后增加较慢。缺血30分钟或更长时间后球囊充气导致左心室壁僵硬度显著降低。缺血60分钟后类似的短暂充气使荧光素钠灌注左心室壁内膜下一半，否则该区域无法进行再灌注。这种无复流现象的逆转伴随着心肌壁僵硬度降低、心肌细胞伸展和心肌毛细血管通畅性增加。
