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EFFECT OF HYDROGEN SULFIDE ON ATRIUM CONTRACTILITY IN CONTROL AND DIABETHIC MICE

https://doi.org/10.20538/1682-0363-2014-6-155-159

Abstract

Hydrogen sulfide (H2S) is endogenously synthesized gasotransmitter that has a regulatory effect in cardiovascular system. Diabetes mellitus leads to an increased risk of hypertension and cardiovascular diseases, so the purpose of the study was to analyze the contractility of the atria mice after application of L-cysteine and H2S. Contractile activity of the myocardium was investigated in the experiment on isolated mouse atria. Alloxan was used for modeling diabetes. Intraperitoneal injection of alloxan resulted in a significant increase of glucose concentration in blood, whereas the concentration of glucose didn’t change at the injection of physiological solution. In control, the addition of NaHS resulted in a significant dose-dependent decrease of the amplitude of contraction of the myocardium, whereas the negative inotropic effect of NaHS was significantly lower in terms of modeling diabetes compare to control conditions. In the control, L-cysteine reduced the amplitude contractions significantly, whereas L-cysteine did not lead to significant changes in the amplitude of contractions in terms of modeling diabetes. These data indicate that the sensitivity of mice’s atria reduced for H2S and L-cysteine in diabetes mellitus.

About the Authors

A. S. Lifanova
Kazan Federal University, Kazan
Russian Federation
Lifanova Anastasia S. 


O. V. Yakovleva
Kazan Federal University, Kazan
Russian Federation
Yakovleva Olga V.


A. I. Zefirov
Kazan State Medical University, Kazan
Russian Federation
Zefirov Andrey L.


G. F. Sitdikova
Kazan Federal University, Kazan
Russian Federation
Sitdikova Guzel F.


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Review

For citations:


Lifanova A.S., Yakovleva O.V., Zefirov A.I., Sitdikova G.F. EFFECT OF HYDROGEN SULFIDE ON ATRIUM CONTRACTILITY IN CONTROL AND DIABETHIC MICE. Bulletin of Siberian Medicine. 2014;13(6):155-159. (In Russ.) https://doi.org/10.20538/1682-0363-2014-6-155-159

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ISSN 1682-0363 (Print)
ISSN 1819-3684 (Online)