Impaired Nongas Exchange Functions of the Lung and Their Role in the Development of Acute Respiratory Distress Syndrome in Severe Brain Injury

Abstract

The study was undertaken to examine the impact of the lung on the content of adrenaline, noradrenaline, serotonin, and lactic acid in systemic blood flow and to define their contribution to the development of acute respiratory distress syndrome (ARDS) in severe brain injury (SBI). Forty victims with severe brain injury were examined. A study group comprised 26 patients. On admission, the patients were found to have ARDSj, later on 12 patients of them were observed to have its progression and to develop pneumonia in its presence. A control group included 14 victims. There were no postoperative complications. During 7 days after brain injury, the time course of changes were determined in the mixed venous (pulmonary arterial) and arterial (femoral arterial) levels of adrenaline and noradrenaline by fluorometry and in those of serotonin and lactic acid by the fluorescence technique [8] and enzymatic assay, respectively. The performed studies have indicated that in SBI, a significant activation of the sympathicoadrenal system results in a noticeable humoral reaction, by increasing the concentration of biologically active substances in the blood flowing to the lung, which leads to a load and subsequent decompensation of nongas exchange functions of the lung in the inactivation of serotonin, noradrenaline, their absorption of lactate, which in the presence of neurodystrophic changes has a great impact on the development of ARDS in victims with SBI. In this case, the clinical, X-ray, and biochemical signs of the development of ARDS appear 12—36 hours after the detected nongas exchange dysfunctions are detectable.