Department of Medical Physics and Informatics, University of Szeged, 9 Koranyi fasor, Szeged, H-6720, Hungary.
Department of Anaesthesiology and Intensive Therapy, University of Szeged, 6 Semmelweis Street, Szeged, H 6725, Hungary.
Respir Res. 2020 Apr 9;21(1):82. doi: 10.1186/s12931-020-01334-y.
Diabetes mellitus causes the deterioration of smooth muscle cells and interstitial matrix proteins, including collagen. Collagen and smooth muscle cells are abundant in the lungs, but the effect of diabetes on airway function and viscoelastic respiratory tissue mechanics has not been characterized. This study investigated the impact of diabetes on respiratory function, bronchial responsiveness, and gas exchange parameters.
Rats were allocated randomly to three groups: a model of type 1 diabetes that received a high dose of streptozotocin (DM1, n = 13); a model of type 2 diabetes that received a low dose of streptozotocin with a high-fat diet (DM2, n = 14); and a control group with no treatment (C, n = 14). Forced oscillations were applied to assess airway resistance (Raw), respiratory tissue damping (G), and elastance (H). The arterial partial pressure of oxygen to the inspired oxygen fraction (PaO/FiO) and intrapulmonary shunt fraction (Qs/Qt) were determined from blood gas samples at positive end-expiratory pressures (PEEPs) of 0, 3, and 6 cmHO. Lung responsiveness to methacholine was also assessed. Collagen fibers in lung tissue were quantified by histology.
The rats in groups DM1 and DM2 exhibited elevated Raw, G, H, and Qs/Qt, compromised PaO/FiO, and diminished airway responsiveness. The severity of adverse tissue mechanical change correlated with excessive lung collagen expression. Increased PEEP normalized the respiratory mechanics, but the gas exchange abnormalities remained.
These findings indicate that diabetes reduces airway and lung tissue viscoelasticity, resulting in alveolar collapsibility that can be compensated by increasing PEEP. Diabetes also induces persistent alveolo-capillary dysfunction and abnormal adaptation ability of the airways to exogenous constrictor stimuli.
糖尿病可导致平滑肌细胞和细胞间质蛋白（包括胶原）恶化。胶原和平滑肌在肺部含量丰富，但糖尿病对气道功能和黏弹性呼吸组织力学的影响尚未得到描述。本研究旨在探讨糖尿病对呼吸功能、支气管反应性和气体交换参数的影响。
将大鼠随机分为三组：接受高剂量链脲佐菌素的 1 型糖尿病模型（DM1，n=13）；接受低剂量链脲佐菌素和高脂肪饮食的 2 型糖尿病模型（DM2，n=14）；未治疗的对照组（C，n=14）。应用强迫振荡技术评估气道阻力（Raw）、呼吸组织阻尼（G）和弹性（H）。通过正呼气末压（PEEP）为 0、3 和 6 cmH2O 时的血气样本，测定动脉血氧分压与吸入氧分数（PaO/FiO）和肺内分流分数（Qs/Qt）。还评估了肺对乙酰甲胆碱的反应性。通过组织学量化肺组织中的胶原纤维。
DM1 和 DM2 组大鼠的 Raw、G、H 和 Qs/Qt 升高，PaO/FiO 降低，气道反应性下降。组织力学不良改变的严重程度与肺胶原过度表达相关。增加 PEEP 可使呼吸力学正常化，但气体交换异常仍存在。
这些发现表明，糖尿病降低了气道和肺组织的黏弹性，导致肺泡塌陷，可通过增加 PEEP 来代偿。糖尿病还会引起持续的肺泡毛细血管功能障碍和气道对外源性收缩刺激的异常适应能力。
