David D, Hilewitz H, Rogel S
Circ Shock. 1977;4(2):153-61.
Hypovolemic shock was maintained for 6 hours in dogs in which the heart was hemodynamically protected by a biological model described earlier. Blood of these dogs was exchanged with that of healthy dogs in which myocardial tension and heart rate were continuously monitored. It was found that rate and force of decline in the recipient dog in a fashion similar to the drop in the animal in shock. If, however, the pH of the infused blood was raised to normal, the bradycardia in the recipient dog was prevented but the myocardial depression was not abolished. Administration of aprotinin alone did not prevent the bradycardia or depression of contractility, whereas correction of the pH and treatment with aprotinin not only prevented the decline in both but led also to a transient increase in myocardial tension of the recipient animal. The results seem to indicate that 1) in shock myocardial depression and cardiac slowing are induced by humoral factors transferable by blood to a normal animal, 2) acidity caused the bradycardia but not drop of tension, 3) aprotinin prevents the depression of contractility only in a normal pH medium, and 4) aprotinin may prevent the action of a preformed myocardial depressant factor rather than inhibit its formation.
在采用先前描述的生物模型对心脏进行血流动力学保护的犬只中，维持低血容量性休克6小时。将这些犬只的血液与健康犬只的血液进行交换，同时持续监测健康犬只的心肌张力和心率。结果发现，受体犬的心率和心肌收缩力下降的速率和程度与休克动物相似。然而，如果将输注血液的pH值恢复正常，可防止受体犬出现心动过缓，但心肌抑制并未消除。单独使用抑肽酶不能防止心动过缓或收缩力下降，而纠正pH值并使用抑肽酶进行治疗，不仅可以防止两者下降，还会使受体动物的心肌张力出现短暂升高。这些结果似乎表明：1）在休克状态下，心肌抑制和心率减慢是由可通过血液传递给正常动物的体液因子所诱发的；2）酸性环境导致心动过缓，但不会引起张力下降；3）抑肽酶仅在正常pH值介质中才能防止收缩力下降；4）抑肽酶可能是阻止了预先形成的心肌抑制因子的作用，而不是抑制其形成。
