Effects of Endothelin-1 and nitric oxide levels on myocardial ischemia-reperfusion injury.

Abstract

To study the role of nitric oxide (NO) in myocardial ischemia-reperfusion injury (IRI) and Endothelin-1 (ET-1) in the process of reperfusion in an animal model. ET is a strong vasoconstrictor peptide, which is closely related to the physiological and pathological state of the cardiovascular system. ET not only directly stimulates and activates a variety of hormones and cytokines, but also is one of the mediators promoting myocardial remodeling, and participates in and promotes myocardial ischemia injury. Before myocardial ischemia, Krebs-Henseleit (KH) perfusion solution containing different concentrations of L-arginine (LA; substrate of NO) were given to 6 groups of rats, and ET was given at the early stage of reperfusion in 3 groups. During reperfusion, cardiac function indexes, myocardial enzyme release and NO content in coronary effluent, and the cardiac malondialdehyde (MDA) content was measured. The myocardial ultrastructure was observed by microscopy. Data of each group are expressed as mean ± standard deviation, and the baseline value of each group before ischemia was the recovery value during reperfusion. SPSS26.0 (IBM, Chicago, USA) was used for statistical processing. Before myocardial ischemia, infusion of KH solution containing a low concentration of LA (10 mmol/L) reduced myocardial IRI, whereas infusion of a KH solution containing high concentration of LA (100 mmol/L) before ischemia significantly aggravated myocardial IRI. The administration of KH solution containing LA and ET-1 (1,000 mmol/L) significantly reduced myocardial IRI. NO plays a dual role in myocardial ischemia-reperfusion, both beneficial and harmful. The combination of NO and ET-1 can reduce the toxic effect of NO.