Taylor, Bryan Joseph

Background Increased pulmonary capillary pressure and a possible desensitization of lung β 2 adrenergic receptors (β 2 AR) involved in fluid removal mechanisms may increase extravascular lung water (E LW ) in stable heart failure (HF) patients. Whether these patients exhibit increased E LW remains controversial. Purpose To determine if HF patients have elevated E LW versus controls (CTL) and if acute β 2 AR agonist inhalation stimulates fluid removal. Methods/Results 14 stable HF patients and 19 healthy age/gender matched CTL were studied. Lung tissue volume (V tis ) (includes tissue, blood and water) and pulmonary capillary blood volume (Vc) were assessed pre and post nebulized albuterol via CT and rebreathe, respectively. E LW was derived as V tis – Vc. Pre albuterol, E LW was greater in HF vs. CTL (861±241 vs. 739±143 ml, P <0.01), with no difference in V tis (938±246 vs. 830±151 ml, P =0.08). Albuterol decreased V tis (–4±2%, P =0.02) but did not change E LW (739±143 vs. 724±132 ml) ( P >0.05) in CTL. In HF, albuterol decreased both V tis (–5±3%) and E LW (– 4±2%) ( P <0.05). There was a negative relationship between baseline values and the pre to post albuterol change for V tis ( r 2 =0.38) and E LW ( r 2 =0.42) ( P <0.01) in HF. Conclusion Lung fluid is elevated in stable HF patients relative to healthy subjects. Stimulation of β 2 ARs appears to enhance fluid removal in HF, especially in patients with elevated lung water at rest.

Background Exposure to hypoxia causes pulmonary vasoconstriction (HPV) and may contribute to the pathogenesis of HAPE. The site of HPV, however, is controversial. While the majority of data suggests HPV occurs in the pulmonary arterioles (precapillary), there is evidence that HPV may also occur in postcapillary vessels. Expansion of pulmonary capillary blood volume (Vc) is primarily passive and thus closely linked to cardiac output (Q). Purpose To examine relationships between Q and Vc during exposure to hypoxia and fluid loading. Methods/Results Healthy adults (n=25, age=31±2 yr) reported to the lab for 2 exposures: 1) 17‐h 12.5% F I O 2 in a hypoxia tent, and 2) fluid loading using IV saline (30 ml/kg over ~15 min). Q, Vc and Dm (alveolar‐capillary conductance) were measured using a rebreathe method with small amounts of C 2 H 2 , CO and NO gas. Saline infusion caused an increase in Q (32±6%, P <0.01) and Vc (39±13%, P <0.05), and a decrease in Dm (−9±3%, P <0.05). Vc/Q was not different pre‐ vs post‐saline (17±2 vs 18±3, P =0.40). Hypoxic exposure caused an increase in pulmonary arterial pressure (67±11%, P <0.01), Vc (57±20%, P =0.04) and Dm (35±6%, P <0.01) despite no change in Q (0.2±2.8%, P =0.98). Vc/Q was greater post‐ vs. pre‐hypoxia (24±4 vs. 17±2, P =0.06). Conclusion The rise in Vc with a constant Q during hypoxic exposure suggests a post capillary site for HPV causing the expansion of the pulmonary capillary bed. HL71478.