No abstract

We measured the uptake of the soluble inert gas dimethyl ether (DME) from a segment of the conducting airways to estimate mucosal blood flow (Qaw) noninvasively. The subjects inhaled, from the functional residual capacity position, a 300-ml gas mixture containing 35% DME, 8% helium, 35% oxygen, and the balance nitrogen; they held their breath for 5 s and then exhaled into a spirometer. During exhalation, the instantaneous concentrations of DME and helium were recorded together with expired gas volume. The maneuver was repeated with breathhold times of 5, 10, 15, and 20 s. We calculated Qaw using the time-dependent decrease in DME concentration in relation to the helium concentration in an expired volume fraction between 80 and 130 ml (representing an anatomic dead-space segment distal to the glottis) and the mean DME concentration. In 10 healthy nonsmokers, mean (+/- SE) Qaw was 8.0 +/- 1.3 ml/min, or 8 +/- 2 microliters/min/cm2 mucosal surface. We obtained a value of 12 +/- 3 microliters/min/cm2 in a validation experiment in sheep. Inhaled methoxamine (nebulized dose 10 mg) caused a 65 +/- 19% decrease (p < 0.05), and albuterol (nebulized dose 2.5 mg) a 92 +/- 17% increase (p < 0.05), in mean Qaw in seven subjects, with the maximum changes occurring immediately or 15 min postinhalation. We conclude that the DME uptake method is an acceptable noninvasive means of estimating airway mucosal blood flow in humans and its modification by vasoactive substances.

Airway edema has been described in heart failure, and, in animal experiments, airway narrowing was observed with elevated left atrial pressure (Pla). On the basis of double-indicator-dilution principles using helium and dimethylether, we were able to measure a water compartment of the tracheal mucosa (VH2O) in dogs. Hypervolemia with an attendant increase in Pla caused by infusion of 2 liters of dextran increased VH2O from 368 +/- 71 (SE) to 794 +/- 177 microliters (P < 0.01). Pulmonary arterial wedge and central venous pressures (Pcv) rose concomitantly. Increases in pulmonary arterial wedge and Pcv by a left atrial balloon catheter produced similar increases in VH2O, whereas increases in Pcv alone by a right atrial balloon did not increase VH2O. Increasing VH2O by dextran infusion was associated with an increase in pulmonary resistance from 1.16 +/- 0.19 to 2.15 +/- 0.24 cmH2O.l-1.s (P < 0.01). These observations show that fluid accumulation in the lung during pulmonary congestion also involves extraparenchymal airways and is related to Pla rather than right atrial pressure. This indicates that sufficient collateral drainage exists during right-sided but not left-sided pressure elevations.