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Obesity and diabetes: similar respiratory mechanical, but different gas exchange defects
American Journal of Physiology-Lung Cellular and Molecular Physiology ( IF 3.6 ) Pub Date : 2020-12-02 , DOI: 10.1152/ajplung.00439.2020
Roberta Sudy 1 , Ferenc Petak 2 , Liliana Kiss 3 , Adam Laszlo Balogh 4 , Gergely H. Fodor 5 , Anita Korsos 3 , Almos Schranc 2 , Barna Babik 6
Affiliation  

Diabetes mellitus increases smooth muscle tone and causes tissue remodelling affecting elastin and collagen. Since lung is dominated by these elements, diabetes is expected to modify the airway function and respiratory tissue mechanics. Therefore, we characterized the respiratory function in patients with diabetes with and without associated obesity. Mechanically ventilated patients with normal body shapes were divided into the control non-diabetic (n=73) and diabetic (n=31) groups. The other two groups included obese patients without diabetes (n=43) or with diabetes (n=30). The mechanical properties of the respiratory system were determined by forced oscillation technique. Airway resistance (Raw), tissue damping (G), and tissue elastance (H) were assessed by forced oscillation. Capnography was applied to determine phase 3 slopes and dead space indices. The intrapulmonary shunt fraction (Qs/Qt) and the lung oxygenation index (PaO2/FiO2) were estimated from arterial and central venous blood samples. Compared with the corresponding control groups, diabetes alone increased the Raw (7.6 ± 6 cmH2O.s/l vs. 3.1 ± 1.9 cmH2O.s/l), G (11.7 ± 5.5 cmH2O/l vs. 6.5 ± 2.8 cmH2O/l), and H (31.5 ± 11.8 cmH2O/l vs. 24.2 ± 7.2 cmH2O/l, (p < 0.001 for all). Diabetes increased the capnographic phase 3 slope, whereas PaO2/FiO2 or Qs/Qt were not affected. Obesity alone caused similar detrimental changes in respiratory mechanics and alveolar heterogeneity, but these alterations also compromised gas exchange. We conclude that diabetes-induced intrinsic mechanical abnormalities are counterbalanced by hypoxic pulmonary vasoconstriction, which maintained intrapulmonary shunt fraction and oxygenation ability of the lungs.

中文翻译:

肥胖和糖尿病:呼吸机械相似,但气体交换缺陷不同

糖尿病会增加平滑肌的张力,并导致组织重构,影响弹性蛋白和胶原蛋白。由于肺由这些元素决定,糖尿病有望改变呼吸道功能和呼吸组织力学。因此,我们对患有和不伴有肥胖症的糖尿病患者的呼吸功能进行了表征。身体形状正常的机械通气患者分为非糖尿病对照组(n = 73)和糖尿病组(n = 31)。其他两组包括没有糖尿病(n = 43)或患有糖尿病(n = 30)的肥胖患者。呼吸系统的机械性能通过强制振荡技术确定。通过强制振荡评估气道阻力(Raw),组织阻尼(G)和组织弹性(H)。应用二氧化碳分析仪确定第3阶段的坡度和死区指数。肺内分流分数(Qs / Qt)和肺氧合指数(PaO2 / FiO 2)是从动脉和中央静脉血样本中估计的。与相应的对照组相比,单独的糖尿病增加了原始水平(7.6±6 cmH 2 O.s / l对3.1±1.9 cmH 2 O.s / l),G(11.7±5.5 cmH 2 O / s对6.5±2.8 cmH 2 O /升),和H(31.5±11.8 CMH 2 O / L比24.2±7.2 CMH 2 O /升,(p <0.001对所有)。糖尿病增加了二氧化碳描记相3斜率,而氧分压2 /氧合指数2或Qs / Qt不受影响。仅肥胖症就引起呼吸力学和肺泡异质性的相似有害变化,但是这些变化也损害了气体交换。我们得出的结论是,低氧性肺血管收缩可以平衡糖尿病引起的内在机械异常,后者可以保持肺内分流分数和肺的氧合能力。
更新日期:2020-12-03
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