Might a high hemoglobin mass be involved in non-cardiogenic pulmonary edema? The case of the chronic maladaptation to high-altitude in the Andes.

Exposure to hypoxic environments when ascending at high altitudes may cause life-threatening pulmonary edema (HAPE) due to a rapid accumulation of extracellular fluid flooding in the pulmonary alveoli. In Andeans, high-altitude adaptation occurs at the expense of being more prone to chronic mountain sickness: relative hypoventilation, excess pulmonary hypertension, and secondary polycythemia. Because HAPE prevalence is high in the Andes, we posit the hypothesis that a high hemoglobine mass may increase HAPE risk. In support of it, high intrapulmonary hypertension along with hyperviscosity produced by polycytemia may enhance sear forces and intravascular hemolysis, thus leading to increased acellular hemoglobin and the subsequent damage of the alveolar and endothelial barrier. It is proposed to investigate the relationship between the vaso-endothelial homeostasis and erythropoiesis in the maladaptation to high altitude and HAPE. This research is especially important when reentry HAPE, since rheologic properties of blood changes with rapid ascent to high altitudes.