Humoral factors in shock causing bradycardia and myocardial depression.
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.
Humoral factors in shock causing bradycardia and myocardial depression. 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.