Interrelationship of Liver Perfusion, Bacteremia and VDM in Hemorrhagic Hypotensive Shock

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Abstract
Normotesnive donor animals perfused the liver of a shock animal with arterial blood. To eliminate any possible contribution by the donor dog, a no. of auto-liver perfusion expts. were carried out. Certain other variables which might account for the beneficial effects of liver perfusion were also investigated. (1) Inhibition of bacterial growth did not appear to be responsible for the beneficial effects of liver perfusion, nor was the growth of bacteria responsible for vascular collapse and death, since the majority of blood cultures obtained from control expts. were sterile, while most of the cultures obtained from the liver perfused animals showed growth of various types of organisms. In spite of this, liver perfused animals were most resistant to the onset of irreversible shock and death. Positive cultures showed no correlation with the vascular state of the animals. (2) Using the Chambers and Zweifach rat mesoappendix technique, assays were carried out for both in morphine and in pentobarbital anesthetized dogs. These substances were not found except in a few isolated instances and when found did not usually correlate with the peripheral vascular state of the shock animal. It was concluded that: liver perfusion with arterial blood during drastic hypotension, whether by means of a donor animal or by the animal itself, will significantly delay but not prevent the onset of irreversible shock; inhibition in the liver of bacterial growth and of the release of VDM is not the mechanism responsible for the beneficial effect of liver perfusion; and neither bacterial growth nor the release of VDM is responsible for the vascular collapse and death that occur following hemorrhagic hypotensive shock.