Meerson F Z, Evsev'eva M E, Abdikaliev N A
Biull Eksp Biol Med. 1984 Jan;97(1):19-22.
The coronary blood flow and heart contractile function were studied on rats with phenylhydrazine-induced chronic hemolytic anemia. The coronary blood flow in the animals' hearts was increased 2.5-fold, whereas the main parameters of contractile function were reduced but insignificantly. After the coronary blood flow dropped to the control level, the pressure and contraction rate fell by 40% and the relaxation rate diminished 2-fold. Thus, the enhanced coronary blood flow in the hearts of animals with hemolytic anemia appears to be a factor that compensates for the maintenance of myocardial contractility at the subnormal level. Administration of the antioxidant ionol, an inhibitor of lipid peroxidation, coupled with phenylhydrazine did not prevent the development of anemia but made the coronary blood flow descend in the hearts of anemic animal only by 80%. Since the iron-containing products of red cell dissolution activate lipid peroxidation during hemolytic anemia, this might play a role in the occurrence of heart muscle injuries. It is suggested that ionol prevents such injuries to a considerable extent, thereby preventing the development of compensatory enhancement of the coronary blood flow and heart contractile function disturbances during its normalization.
对苯肼诱导的慢性溶血性贫血大鼠的冠状动脉血流量和心脏收缩功能进行了研究。动物心脏的冠状动脉血流量增加了2.5倍，而收缩功能的主要参数有所降低，但不显著。冠状动脉血流量降至对照水平后，压力和收缩率下降了40%，舒张率降低了2倍。因此，溶血性贫血动物心脏中增强的冠状动脉血流量似乎是在亚正常水平维持心肌收缩力的一个补偿因素。抗氧化剂离子醇（一种脂质过氧化抑制剂）与苯肼联合给药并不能预防贫血的发生，但仅使贫血动物心脏中的冠状动脉血流量下降了80%。由于红细胞溶解产生的含铁产物在溶血性贫血期间会激活脂质过氧化，这可能在心肌损伤的发生中起作用。有人认为，离子醇在很大程度上可预防此类损伤，从而在冠状动脉血流量正常化过程中防止代偿性增强和心脏收缩功能紊乱的发生。
