Some Enzymatic Aspects of Hemorrhagic Shock

Abstract

Since a half century, a multiplicity of metabolic alterations has been described following injury and shock. In clinically, physicians are obliged to determine whether the patients recover or die from the shock. Attention has been drawn to the metabolic changes after the shock. Until fairly recently, the majority of such studies has dealt with chemical changes in the blood and urine, because of the ease of obtaining such samples from living animals and patients for analysis, and difficulty of obtaining tissue samples from patients. Many questions are remained wether the analysis of chemical changes of blood and urine reflects the biochemical change of the tissue and cell. Only a few attempt has been made to study the problems of the cellular and subcellular biochemical changes following shock in vivo and in vitro. Main factor which affects the metabolic changes in tissue after shock is obviously anoxia due to the incompleteness of effective blood flow. Hypoxia and anoxia not only proceed the alteration of oxidative reaction but also destruct the cell membrane and the structure of the cells. Metabolic alterations of shock due to the impairment of tissue perfusion are reported and reviewed [1–3]. By the shock, the oxidation-reduction potential shifts toward reduced state, and an accumulation of undisposable lactic acid is observed.