Chance William W, Rhee Chanhaeng, Yilmaz Cuneyt, Dane D Merrill, Pruneda M Lourdes, Raskin Philip, Hsia Connie C W
Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Diabetes Care. 2008 Aug;31(8):1596-601. doi: 10.2337/dc07-2323. Epub 2008 May 20.
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.
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.
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.
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.
1型糖尿病患者存在肺泡微血管功能中度受损，表现为肺容积和弥散能力（DL(CO)）受限。我们研究了2型糖尿病患者是否也会出现类似的损伤，并确定损伤的生理来源以及与血糖和全身微血管病变的关系。
在一所大学附属糖尿病治疗中心和门诊糖尿病诊所进行了一项横断面研究，纳入了69例无明显心肺疾病的非吸烟2型糖尿病患者。测定了静息和运动时的肺容积、肺血流量（Q）、DL(CO)、膜弥散能力（通过一氧化氮摄取量测定[DL(NO)]）和肺毛细血管血容量（V(C)），并与45例健康非吸烟者以及正常参考值进行比较。
与对照组相比，2型糖尿病患者运动时的摄氧量、Q以及DL(CO)、DL(NO)和V(C)的峰值水平降低了10% - 25%。在非肥胖患者（BMI <30 kg/m²）中，DL(CO)、DL(NO)和V(C)的降低完全由较低的肺容积和峰值Q所解释，但这些因素并不能完全解释肥胖患者（BMI >30 kg/m²）的损伤情况。无论BMI如何，患者V(C)相对于Q增加的斜率降低了约20%，这与肺泡 - 毛细血管募集受损一致。功能损伤以性别特异性方式与糖化血红蛋白水平、视网膜病变、神经病变和微量白蛋白尿直接相关。
2型糖尿病患者的肺泡微血管储备减少，反映了肺容积、肺泡灌注和毛细血管募集受限。这种减少与血糖控制和肺外微血管病变相关，且肥胖会使其加重。
