title: Diminished alveolar microvascular reserves in type 2 diabetes reflect systemic microangiopathy.
abstract: OBJECTIVE
  Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DL(CO)). 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.
  
  
  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 (Q), DL(CO), membrane diffusing capacity (measured from nitric oxide uptake [DL(NO)]), and pulmonary capillary blood volume (V(C)) 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, Q and DL(CO), DL(NO), and V(C) at exercise were 10-25% lower compared with those in control subjects. In nonobese patients (BMI <30 kg/m(2)), reductions in DL(CO), DL(NO), and V(C) were fully explained by the lower lung volume and peak Q, but these factors did not fully explain the impairment in obese patients (BMI >30 kg/m(2)). The slope of the increase in V(C) with respect to Q was reduced approximately 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.
authors.affiliation: Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas, USA.
authors.forename: William W
authors.initials: WW
authors.lastname: Chance
authors.forename: Chanhaeng
authors.initials: C
authors.lastname: Rhee
authors.forename: Cuneyt
authors.initials: C
authors.lastname: Yilmaz
authors.forename: D Merrill
authors.initials: DM
authors.lastname: Dane
authors.forename: M Lourdes
authors.initials: ML
authors.lastname: Pruneda
authors.forename: Philip
authors.initials: P
authors.lastname: Raskin
authors.forename: Connie C W
authors.initials: CC
authors.lastname: Hsia
mesh_terms: D000114:Acetylene / Q000032:analysis; D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D015992:Body Mass Index; D001944:Breath Tests; D002248:Carbon Monoxide / Q000032:analysis; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008176:Lung Volume Measurements; D008297:Male; D008697:Methane / Q000032:analysis; D008833:Microcirculation / Q000502:physiology*; D008875:Middle Aged; D010101:Oxygen Consumption; D011650:Pulmonary Alveoli / Q000098:blood supply*; D011652:Pulmonary Circulation; D011653:Pulmonary Diffusing Capacity / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents; D007004:Hypoglycemic Agents; D000960:Hypolipidemic Agents; D002248:Carbon Monoxide; D000114:Acetylene; D008697:Methane