Pulmonary Gas Exchange Abnormalities Following Intravascular Coagulation Reticuloendothelial Involvement

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Abstract
The influence of RES 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 RES blockade resulted in a significant (P < 0.05) elevation in pulmonary vascular resistance which was transient and returned to prechallenge levels over a 2-4 h period. This response was not associated with any significant change in physiological dead space. In contrast, intravascular coagulation in the presence of RES blockage resulted in significant (P < 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 after thrombin infusion during RES blockade suggest a functional role for the RES 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.