Involvement of myocardial acute stretch-induced ROS production in development of heart failure

• Published in: Transactions of Japanese Society for Medical and Biological Engineering Vol. Annual58; no. Abstract; p. 332
• Main Authors: KAIHARA, KEIKO, Naruse, Keiji, Iribe, Gentaro
• Format: Journal Article
• Language: Japanese
• Published: Japanese Society for Medical and Biological Engineering 2020
• ISSN: 1347-443X; 1881-4379
• DOI: 10.11239/jsmbe.Annual58.332

Myocardial acute stretch increases NADPH oxidase (NOX) 2-derived ROS production to modulate Ca2+ handling in intact ventricular cardiomyocytes. However, their behaviors in failing heart are unclear. In this study, we investigate the stretch-induced change in ROS production in pressure overload-induced cardiac failure in mice. Heart failure was induced via chronic Transverse Aortic Constriction (TAC). The isolated cardiomyocytes loaded with 2`,7`-Dichlorodihydrofluorescein were exposed to 8% axial stretch using carbon fiber technique, to observe stretch-induced ROS production. Cellular contractility was estimated by slopes of end-systolic force-length relation (ESFLR) curves.Although the slope of ESFLR showed a significant decrease after TAC, neither base nor stretch-induced change in ROS production were significantly affected by TAC. Despite clinical significance of ROS in the progression of heart failure, the present results showed that response of NOX2 to stretch is not involved with underlying mechanisms of progression of TAC-induced myocardial dysfunction.