Abstract
Summary
In vitro studies have shown that the vasodepressor principle, which appears during the hypo-reactive stage of shock and results from the anoxia of liver and skeletal muscles, can be inactivated under aerobic conditions by healthy liver slices. The present study was concerned with the mechanisms by which endogenous and exogenous VDM are removed from the circulation of the living animal. The exogenous VDM was concentrated and purified from saline extracts of anaerobic beef liver. The endogenous VDM was released into the blood following liver anoxia produced by temporary occlusion of the hepatic artery in a partially eviscerated preparation. Two mechanisms for VDM removal were revealed:
(1) its inactivation by the healthy liver;
(2) its excretion into the urine by the normal kidney. A preliminary period of hepatic anoxia rendered the liver incapable of inactivating VDM in vivo, presumably through anoxic damage to the hepatic enzyme system for this function. This situation is analogous to the progressive impairment of the VDM inactivating mechanism in the liver which develops during the course of shock and which is considered responsible for the perpetuation of the hypo-reactive state of the peripheral vascular system. The loss of the renal excretory function for VDM during hypo-reactive shock deprives the animal of an important means of clearing the blood of VDM and thereby aiding in liberating the vascular bed from this decompensatory vasotropic principle.
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