Journal
JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE
Volume 10, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/jcdd10030103
Keywords
low-molecular weight heparin; enoxaparin; cardiac ischemia/reperfusion; cardiac arrhythmias; purinergic signaling
Categories
Ask authors/readers for more resources
The study investigates the pharmacological modulation of adenosine signaling in cardiac cells by enoxaparin in the treatment of acute myocardial infarction (AMI). The results show that enoxaparin reduces the incidence of ventricular arrhythmias and atrioventricular block induced by cardiac ischemia and reperfusion (CIR), suggesting a promising cardioprotective strategy in AMI therapy by targeting the ADO signaling pathway.
Background: Although several studies suggest that heparins prevent arrhythmias caused by acute myocardial infarction (AMI), the molecular mechanisms involved remain unclear. To investigate the involvement of pharmacological modulation of adenosine (ADO) signaling in cardiac cells by a low-molecular weight heparin (enoxaparin; ENOX) used in AMI therapy, the effects of ENOX on the incidences of ventricular arrhythmias (VA), atrioventricular block (AVB), and lethality (LET) induced by cardiac ischemia and reperfusion (CIR) were evaluated, with or without ADO signaling blockers. Methods: To induce CIR, adult male Wistar rats were anesthetized and subjected to CIR. Electrocardiogram (ECG) analysis was used to evaluate CIR-induced VA, AVB, and LET incidence, after treatment with ENOX. ENOX effects were evaluated in the absence or presence of an ADO A1-receptor antagonist (DPCPX) and/or an inhibitor of ABC transporter-mediated cAMP efflux (probenecid, PROB). Results: VA incidence was similar between ENOX-treated (66%) and control rats (83%), but AVB (from 83% to 33%) and LET (from 75% to 25%) incidences were significantly lower in rats treated with ENOX. These cardioprotective effects were blocked by either PROB or DPCPX. Conclusion: These results indicate that ENOX was effective in preventing severe and lethal arrhythmias induced by CIR due to pharmacological modulation of ADO signaling in cardiac cells, suggesting that this cardioprotective strategy could be promising in AMI therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available