Diminished Alveolar Microvascular Reserves in Type 2 Diabetes Reflect Systemic Microangiopathy

  1. William W. Chance, MSEE,
  2. Chanhaeng Rhee, MD,
  3. Cuneyt Yilmaz, PHD,
  4. D. Merrill Dane, MS,
  5. M. Lourdes Pruneda, MSN,
  6. Philip Raskin, MD and
  7. Connie C.W. Hsia, MD
  1. From the Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas
  1. Corresponding author: Connie C.W. Hsia, connie.hsia{at}utsouthwestern.edu

Abstract

OBJECTIVE—Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DLCO). We examined whether similar impairment develops in type 2 diabetes and defined the physiologic sources of impairment as well as the relationships to glycemia and systemic microangiopathy.

RESEARCH DESIGN AND METHODS—A cross-sectional study was conducted at a university-affiliated diabetes treatment center and outpatient diabetes clinic, involving 69 nonsmoking type 2 diabetic patients without overt cardiopulmonary disease. Lung volume, pulmonary blood flow (Q̇), DLCO, membrane diffusing capacity (measured from nitric oxide uptake [DLNO]), and pulmonary capillary blood volume (VC) were determined at rest and exercise for comparison with those in 45 healthy nonsmokers as well as with normal reference values.

RESULTS—In type 2 diabetic patients, peak levels of oxygen uptake, Q̇ and DLCO, DLNO, and VC at exercise were 10–25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m2), reductions in DLCO, DLNO, and VC were fully explained by the lower lung volume and peak Q̇, but these factors did not fully explain the impairment in obese patients (BMI >30 kg/m2). The slope of the increase in VC with respect to Q̇ was reduced ∼20% in patients regardless of BMI, consistent with impaired alveolar-capillary recruitment. Functional impairment was directly related to A1C level, retinopathy, neuropathy, and microalbuminuria in a sex-specific manner.

CONCLUSIONS—Alveolar microvascular reserves are reduced in type 2 diabetes, reflecting restriction of lung volume, alveolar perfusion, and capillary recruitment. This reduction correlates with glycemic control and extrapulmonary microangiopathy and is aggravated by obesity.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 20 May 2008.

    The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the National Institute of Diabetes and Digestive and Kidney Diseases or of the National Institutes of Health. The funding sources had no role in the conduct of the study or in the decision to submit the manuscript for publication.

    Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Received December 14, 2007.
    • Accepted May 8, 2008.
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