Endotoxin‐Induced Intravascular Coagulation and Shock in Dogs: The Role of Factor VII

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Abstract
Summary. Endotoxin (E. coli 0111; 2.5 mg/kg) was given via an aortic cannula to groups of normal and factor‐VII deficient dogs to determine whether factor‐VII deficiency afforded protection against endotoxin‐induced shock and intravascular coagulation. Normal dogs showed the dramatic fall in blood pressure characteristic of endotoxin shock and became deeply unconscious throughout the 5 hr period of the experiment. The factor‐VII deficient dogs had a niarkedly less dramatic response. The fall in blood pressure was significant but only transitory and the dogs required additional anaesthesia. Endotoxin‐induced intravascular coagulation occurred in both normal and factor‐VII deficient dogs. However, the decrease in factor‐V activity was greater, and the platelets returned to normal levels more slowly, in normal dogs than in factor‐VII deficient dogs. Plasminogen levels fell significantly in normal dogs, but not in the factor‐VII deficient animals. Autopsies revealed marked differences between the groups. Fibrin‐containing thrombi were regularly observed in normal dogs, but in factor‐VII deficient dogs such lesions were absent or minimal. Hereditary factor‐VII deficiency may therefore afford protection against endotoxin‐induced shock and intravascular coagulation. The difference in intravascular coagulation may explain the modified shock response in factor‐VII deficient dogs or vice versa, but convincing evidence for a causal relationship has not yet been collected.

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