[Role of changes in insulin-binding activity and energy metabolism in the pathogenesis of experimental crush syndrome].

Study of the effect of the crush syndrome on cell metabolism and insulin-binding activity revealed a new aspect of the pathogenesis of the syndrome, namely, a marked reaction of the mononuclear receptor apparatus. Accumulation of lactate in the tissues and the development of acidosis probably play an important role in disturbance of the insulin-binding activity of the plasma membrane. Reduction of the level of tree adenine nucleotides and ATP in particular may be of essential importance in the late stages of compression. Of importance in the pathogenesis of the crush syndrome was the binding of insulin with its receptors and the subsequent intensification of metabolic disorders and reduction of phosphorylation, which in turn may be the cause of reduced transmission of the signal to the receptors, i. e. disorder of the postreceptor action of insulin.