Pulmonary capillary recruitment in response to hypoxia in healthy humans: A possible role for hypoxic pulmonary venoconstriction?

作者：Taylor Bryan J^*; Kjaergaard Jesper; Snyder Eric M; Olson Thomas P; Johnson Bruce D

来源：Respiratory Physiology & Neurobiology, 2011, 177(2): 98-107.

DOI：10.1016/j.resp.2011.04.005

• Hypoxic pulmonary vasoconstriction
• Pulmonary capillary blood volume
• Cardiac output
• Pulmonary artery pressure
• Left ventricular diastolic function

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 similar to 15 min) or 17-h normobaric hypoxia (FIO2 = 12.5%). Cardiac output ((Q)) over dot 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 (Q) over dot and Vc (P < 0.05) with no change in Vc/(Q) over dot (P = 0.97). Hypoxic-exposure increased Vc (P < 0.01) despite no change in (Q) over dot (P = 0.25), increased sPpa (P < 0.01), and impaired LV relaxation. Multiple regression suggested that similar to 37% of the hypoxia-mediated increase in Vc was attributable to alterations in (Q) over dot, sPpa and LV diastolic function. In conclusion, hypoxia-induced pulmonary capillary recruitment in humans is only partly accounted for by changes in (Q) over dot, sPpa and LV diastolic function. We speculate that hypoxic pulmonary venoconstriction may play a role in such recruitment.

• 出版日期2011-7-31