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Genetic variation of the ₂-adrenergic receptor is associated with differences in lung fluid accumulation in humans

Departments of ¹Internal Medicine and ²Anesthesiology, Mayo Clinic, Rochester, Minnesota; and the ³Division of Physiological Imaging, University of Iowa, Iowa City, Iowa

Submitted 16 November 2006 ; accepted in final form 5 March 2007

The ₂-adrenergic receptors (₂AR) play an important role in lung fluid regulation. Previous research has suggested that subjects homozygous for arginine at amino acid 16 of the ₂AR (Arg16) may have attenuated receptor function relative to subjects homozygous for glycine at the same amino acid (Gly16). We sought to determine if the Arg16Gly polymorphism of the ₂AR influenced lung fluid balance in response to rapid saline infusion. We hypothesized that subjects homozygous for Arg at amino acid 16 (n = 14) would have greater lung fluid accumulation compared with those homozygous for Gly (n = 15) following a rapid intravenous infusion of isotonic saline (30 ml/kg over 17 min). Changes in lung fluid were determined using measures of lung density and tissue volume (computerized tomography imaging) and measures of pulmonary capillary blood volume (Vc) and alveolar-capillary conductance (D_M, determined from the simultaneous assessment of the diffusing capacities of the lungs for carbon monoxide and nitric oxide). The saline infusion resulted in elevated catecholamines in both genotype groups (Arg16 283 ± 117% vs. Gly16 252 ± 118%, P > 0.05). The Arg16 group had a larger decrease in D_M and increase in lung tissue volume and lung water after saline infusion relative to the Gly16 group (D_M –13 ± 14 vs. 0 ± 26%, P < 0.05; lung tissue volume 13 ± 11 vs. 3 ± 11% and lung water +90 ± 66 vs. +48 ± 144 ml, P = 0.10, P < 0.05, for Arg vs. Gly16, respectively, means ± SD). These data suggest that subjects homozygous for Arg at amino acid 16 of the ₂AR have a greater susceptibility for lung fluid accumulation relative to subjects homozygous for Gly at this position.

pulmonary edema

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