H 2 S donor improves heart function and vascular relaxation in diabetes

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...

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Published in:European journal of clinical investigation Vol. 51; no. 1; p. e13354
Main Authors: Dorofeyeva, Natalya, Drachuk, Konstantin, Rajkumar, Rajasekaran, Sabnis, Omkar, Sagach, Vadim
Format: Journal Article
Language:English
Published: England 01-01-2021
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Abstract 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.
AbstractList 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.
Author Dorofeyeva, Natalya
Sagach, Vadim
Rajkumar, Rajasekaran
Sabnis, Omkar
Drachuk, Konstantin
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32729630$$D View this record in MEDLINE/PubMed
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Keywords nitric oxide
hydrogen sulphide
diabetes
endothelial dysfunction
heart
Language English
License 2020 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.
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