Pulmonary Gas Exchange Abnormalities Following Intravascular Coagulation. Reticuloendothelial Involvement

The influence of reticuloendothelial (RE) blockade on the pulmonary hemodynamic and gas exchange response to thrombin induced low-grade intravascular coagulation was studied in dogs during fibrinolytic inhibition. Neither saline infusion nor experimentally induced RE blockade significantly increased pulmonary vascular resistance, physiologic dead space, or pulmonary venous admixture. Intravascular coagulation in the absence of RE blockade resulted in a significant (p less than 0.05) elevation in pulmonary vascular resistance which was transient and returned to prechallenge levels over a two to four hour period. This response was not associated with any significant change in physiological dead space. In contrast, intravascular coagulation in the presence of RE blockade resulted in significant (p less than 0.05) hemodynamic and gas exchange abnormalities. These included an acute elevation in pulmonary vascular resistance, a decrease in arterial oxygenation, an increase in pulmonary venous admixture, and a sustained elevation in physiologic dead space. These events were associated with an elevation in the lung wet-to-dry weight ratios. Gas exchange and hemodynamic alterations afterthrombin infusion during RE blockade suggest a functional role for the reticuloendothelial system in the prevention of pulmonary injury during intravascular coagulation. Thus, this study suggests a possible role of the RES in minimizing pulmonary injury during states of increased microaggregate formation.