Dorofeyeva Natalya, Drachuk Konstantin, Rajkumar Rajasekaran, Sabnis Omkar, Sagach Vadim
A.A. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
Vellore Institute of Technology, Vellore, India.
Eur J Clin Invest. 2021 Jan;51(1):e13354. doi: 10.1111/eci.13354. Epub 2020 Oct 2.
Diabetes dramatically increases the risk of cardiovascular complications and mortality. Hydrogen sulphide plays an important role in reducing oxidative stress. Several studies demonstrated that hydrogen sulphide protects islet beta cells from oxidant stress damage and decreases apoptosis. The aim of the work is to investigate the effect of hydrogen sulphide donor on heart functions and endothelium-dependent relaxation of aortic smooth muscle in diabetes.
Rats were divided into control and diabetic groups. Diabetes mellitus was induced with a single intraperitoneally injection of streptozotocin (60 mg kg ). The functional cardiohemodynamic indicators were registered via microcatheter and Pressure-Volume System. The sodium hydrosulphide NaHS (15.8 mg kg ) was administered intraperitoneally. The contractile activity of the muscle preparations of the thoracic aorta was recorded using a strain gauge.
We demonstrate that the NaHS improves pumping function and restores diastolic heart function in streptozotocin-induced (STZ) diabetes rats. We show that pretreatment with NaHS increased the stroke volume by 43.1%, and the ejection fraction increased by 48.64%. NaHS improves the ventriculo-arterial coupling and increases by 3.4 times acetylcholine-induced relaxation of the aorta in diabetic rats. The inhibition of NOS activity by blocker L-NAME abolished NaHS-mediated vasodilatation in the intact endothelium of the aorta in diabetes. It indicates that the NaHS caused vasodilatation by a NOS-dependent mechanism.
The exogenous hydrogen sulphide can improve pumping function and restore diastolic heart function in diabetes. The pretreatment with NaHS can prevent endothelial dysfunction in diabetes due to the NOS-dependent mechanism.
糖尿病显著增加心血管并发症和死亡风险。硫化氢在减轻氧化应激方面发挥重要作用。多项研究表明，硫化氢可保护胰岛β细胞免受氧化应激损伤并减少细胞凋亡。本研究旨在探讨硫化氢供体对糖尿病大鼠心脏功能及主动脉平滑肌内皮依赖性舒张的影响。
将大鼠分为对照组和糖尿病组。通过腹腔注射一次链脲佐菌素（60 mg/kg）诱导糖尿病。通过微导管和压力-容积系统记录心脏功能血流动力学指标。腹腔注射硫氢化钠（NaHS，15.8 mg/kg）。使用应变片记录胸主动脉肌肉制剂的收缩活性。
我们证明，NaHS可改善链脲佐菌素诱导的（STZ）糖尿病大鼠的泵血功能并恢复舒张期心脏功能。我们发现，用NaHS预处理可使糖尿病大鼠的每搏输出量增加43.1%，射血分数增加48.64%。NaHS改善心室-动脉耦联，并使糖尿病大鼠主动脉乙酰胆碱诱导的舒张增加3.4倍。在糖尿病大鼠中，用一氧化氮合酶（NOS）抑制剂L-NAME抑制NOS活性可消除NaHS介导的主动脉完整内皮的血管舒张。这表明NaHS通过依赖NOS的机制引起血管舒张。
外源性硫化氢可改善糖尿病大鼠的泵血功能并恢复舒张期心脏功能。用NaHS预处理可通过依赖NOS的机制预防糖尿病中的内皮功能障碍。
