Sagach V F, Dmitrieva A V
Fiziol Zh (1978). 1990 Jul-Aug;36(4):8-14.
Experiments carried out on anesthetized dogs have shown that reperfusion of long-ischemized leg tissues is accompanied by a significant decrease of the cardiac output and myocardial contractility. Restriction of the venous return to the heart is important in the cardiac output decrease due to an increase of venous compliance and blood pooling on the peripheral circulation. The preliminary blockade of platelet-activating factor (PAF) receptors decreases degree of the cardio- and hemodynamic disturbances after reperfusion of ischemized tissues and prevents development of pulmonary hypertension. Similarity of the postreperfusion central and peripheral hemodynamic disturbances and animal responses to injection of the exogenous PAF as well as the presence of the protective effect of PAF-receptor antagonist BNo. 52021 permit concluding, that PAF takes part in the development of postischemic shock reaction and its receptor blockade can be used to prevent postreperfusion hemodynamic disorders.
在麻醉犬身上进行的实验表明，长期缺血的腿部组织再灌注会伴随着心输出量和心肌收缩力的显著下降。由于静脉顺应性增加和外周循环血液淤积导致心输出量减少，限制心脏的静脉回流很重要。血小板活化因子（PAF）受体的预先阻断可降低缺血组织再灌注后心脏和血流动力学紊乱的程度，并防止肺动脉高压的发展。再灌注后中枢和外周血流动力学紊乱与动物对外源性PAF注射反应的相似性，以及PAF受体拮抗剂BNo. 52021的保护作用的存在，使得我们可以得出结论，即PAF参与了缺血后休克反应的发展，其受体阻断可用于预防再灌注后血流动力学紊乱。
