We examined mechanisms by which hypoxia may elicit pulmonary capillary recruitment in humans. On separate occasions, twenty-five healthy adults underwent exposure to intravenous saline infusion (30. ml/kg ∼15. min) or 17-h normobaric hypoxia (FIO2=12.5%). Cardiac output (Q̇) and pulmonary capillary blood volume (Vc) were measured before and after saline infusion and hypoxic-exposure by a rebreathing method. Pulmonary artery systolic pressure (sPpa) and left ventricular (LV) diastolic function were assessed before and after hypoxic-exposure via echocardiography. Saline infusion increased Q̇ and Vc (P< 0.05) with no change in Vc/Q̇ (P = 0.97). Hypoxic-exposure increased Vc (P< 0.01) despite no change in Q̇ (P = 0.25), increased sPpa (P< 0.01), and impaired LV relaxation. Multiple regression suggested that ∼37% of the hypoxia-mediated increase in Vc was attributable to alterations in Q̇, sPpa and LV diastolic function. In conclusion, hypoxia-induced pulmonary capillary recruitment in humans is only partly accounted for by changes in Q̇, sPpa and LV diastolic function. We speculate that hypoxic pulmonary venoconstriction may play a role in such recruitment.
Bibliographical noteFunding Information:
This work was supported by National Heart, Lung, and Blood Institute Grant HL-71478. BJT is supported by a Fulbright Commission UK Distinguished Scholar Award.
- Cardiac output
- Hypoxic pulmonary vasoconstriction
- Left ventricular diastolic function
- Pulmonary artery pressure
- Pulmonary capillary blood volume