Guazzi Marco, Tumminello Gabriele, Matturri Marco, Guazzi Maurizio D
Department of Medicine and Surgery, University of Milan, Cardiology Division, San Paolo Hospital, Milan, Italy.
J Am Coll Cardiol. 2003 Sep 17;42(6):1044-50. doi: 10.1016/s0735-1097(03)00914-8.
This study sought to test whether insulin improves exercise ventilatory efficiency (VE/VCO2 slope) and oxygen uptake at peak exercise (peak VO2) in patients with type 2 diabetes-heart failure (HF) comorbidity.
In type 2 diabetes-HF comorbidity, depression of alveolar-capillary diffusion (DL(CO)) correlates with deterioration of exercise VE/VCO2 slope and peak VO2. Insulin potentiates DL(CO) in these patients.
Exercise ventilatory efficiency and peak VO2 (cycle ergometry ramp protocol), as well as DL(CO) at rest and its subdivisions (membrane conductance [D(M)] and pulmonary capillary blood volume [V(C)]) were assessed in 18 patients with type 2 diabetes-HF comorbidity at baseline and after 50 ml of saline + regular insulin (10 IU), or saline, was infused on consecutive days, according to a random crossover design. Glycemia was kept at pre-insulin level for the experiment duration.
Baseline DL(CO), D(M), peak VO2, and VE/VCO2 slope were compromised in these patients. At measurements performed in the 60 min after infusions, compared with at baseline, saline was ineffective, whereas insulin augmented peak VO2 (+13.5%) and lowered VE/VCO(2) slope (-18%), and also increased time to anaerobic threshold (+29.4%), maximal O2 pulse (+12.3%), aerobic efficiency (+21.2%), DL(CO) (+12.5%), and D(M) (+21.6%), despite a reduction in V(C) (-16.3%); insulin did not vary cardiac index and ejection fraction at rest. Changes in peak VO2 and VE/VCO2 slope (r = 0.67, p = 0.002; r = -0.73, p < 0.001, respectively) correlated with those in DL(CO). These responses were unrelated to glycohemoglobin and baseline fasting blood sugar. They were persistent at 6 h after insulin infusion, and were undetectable at 24 h.
In diabetes-HF comorbidity, insulin causes a prolonged improvement in physical performance through activation of multiple factors, among which facilitation of gas conductance seems to be predominant.
本研究旨在测试胰岛素是否能改善2型糖尿病合并心力衰竭（HF）患者的运动通气效率（VE/VCO2斜率）和运动峰值摄氧量（峰值VO2）。
在2型糖尿病合并HF中，肺泡-毛细血管弥散（DL(CO)）降低与运动VE/VCO2斜率和峰值VO2的恶化相关。胰岛素可增强这些患者的DL(CO)。
根据随机交叉设计，对18例2型糖尿病合并HF患者在基线时以及连续两天输注50 ml生理盐水+正规胰岛素（10 IU）或生理盐水后，评估运动通气效率和峰值VO2（自行车测力计递增方案），以及静息时的DL(CO)及其细分指标（膜传导率[D(M)]和肺毛细血管血容量[V(C)]）。在实验期间，血糖维持在胰岛素注射前的水平。
这些患者的基线DL(CO)、D(M)、峰值VO2和VE/VCO2斜率均受损。在输注后60分钟进行的测量中，与基线相比，生理盐水无效，而胰岛素使峰值VO2增加（+13.5%），VE/VCO(2)斜率降低（-18%），还增加了无氧阈值时间（+29.4%）、最大氧脉搏（+12.3%）、有氧效率（+21.2%）、DL(CO)（+12.5%）和D(M)（+21.6%），尽管V(C)有所降低（-16.3%）；胰岛素对静息时的心指数和射血分数无影响。峰值VO2和VE/VCO2斜率的变化（分别为r = 0.67，p = 0.002；r = -0.73，p < 0.001）与DL(CO)的变化相关。这些反应与糖化血红蛋白和基线空腹血糖无关。它们在胰岛素输注后6小时持续存在，在24小时时无法检测到。
在糖尿病合并HF中，胰岛素通过激活多种因素导致身体机能的长期改善，其中促进气体传导似乎占主导地位。
