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It has been shown that capillary endothelium serves indispensable functions under normal physiologic conditions. These include local capillary hyperemia incident to functional activity of tissue cells, inflammatory hyperemia in response to cellular injury, the processes of diffusion and osmosis both in the distribution of useful substances and in the elimination of wastes. Not the least important function of the endothelial membrane has to do with the mechanism of water balance.
The performance of these functions requires that endothelium be delicately sensitive to oxygen tension, to the presence of metabolites and cytoplasmic substances. This very sensitivity renders endothelium a highly vulnerable structure. Its essential quality of semipermeability and its normal tonus are readily affected by diverse agents. These include lack of oxygen, the presence of metabolites in abnormal concentration, products of tissue injury and protein cleavage, bacterial proteins and toxins, venoms, and various drugs, chemicals, and poisons.
The effects of these and similar agents may cause abnormal permeability of a large area of endothelium. This produces a characteristic clinical syndrome of circulatory disturbance, usually called shock or collapse, accompanied by an equally characteristic group of physiologic disorders. The visceral changes seen at necropsy are those indicative of capillary damage. Hemoconcentration is an associated phenomenon which is highly valuable in the recognition of this syndrome in its early stages.
The action of many drugs, chemicals, and poisons is due in part to their effects upon endothelium. It appears that pharmacologic and toxicologic interpretations may need revision to include the effects of many agents upon capillary endothelium.
The self-perpetuating quality of this type of circulatory deficiency makes early recognition essential to successful management. Hemoconcentration is a more useful index than a decline in arterial blood pressure. The former occurs early and is detectable during the incipient stages, while the latter is a sign that the mechanism of compensation has failed.
Efforts to combat shock will be directed logically toward the removal of the cause, toward the restoration of the lost blood volume and capillary tonus, and toward relieving anoxia.
Unless the condition that caused the circulatory deficiency is relieved, any efforts to restore circulatory efficiency will be useless. Transfusions of plasma or serum are more suitable than whole blood, because they relieve the hemoconcentration by supplying the same type of fluid which was lost. There is physiologic evidence that one function of the adrenal cortical hormone is the maintenance of endothelial tonus. Hence the use of cortical extract during the incipient stages of shock is logical. Recent reports of its use in experimental and in clinical shock indicate beneficial effects. The inhalation of oxygen may retard the progress of the circulatory deficiency, since anoxia supplies the self-perpetuating quality in the mechanism of shock.
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