Faculty, Staff and Student Publications

Language

English

Publication Date

2-1-2025

Journal

Journal of Cellular and Molecular Medicine

DOI

10.1111/jcmm.70412

PMID

39936536

PMCID

PMC11815564

PubMedCentral® Posted Date

2-12-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Del Nido cardioplegia (DNC), a blood-and-crystalloid solution containing high and low concentrations of potassium and calcium, respectively, is used as a single-dose antegrade infusion to induce immediate cardiac arrest in the surgery of patients with cardiovascular diseases requiring extracorporeal circulation. Adding cardioprotective molecules may further reduce the damage-triggered ischemia/reperfusion (I/R) injury. Angiotensin-(1-9) (Ang-(1-9)) and angiotensin-(1-7) (Ang-(1-7)), members of the counter-regulatory renin-angiotensin system, have shown cardioprotective effects in cardiac hypertrophy and I/R models. This study aimed to evaluate the effects of Ang-(1-9) and Ang-(1-7), as adjuvants of the DNC, on cardioprotection and ventricular function in isolated rat hearts subjected to I/R and in cultured neonatal rat ventricular myocytes subjected to simulated I/R (sI/R). The addition of DNC and Ang-(1-9) and Ang-(1-7) decreased lactic dehydrogenase (LDH) release in cultured cardiomyocytes subjected to sI/R in comparison to those cardiomyocytes subjected to sI/R and incubated with DNC alone. Moreover, hearts treated with Ang-(1-9) during reperfusion after DNC + I/R exhibited fewer arrhythmias and required less time to reach left ventricular developed pressure stability. Overall, reperfusion with DNC and Ang-(1-9) improves the recovery of the left ventricular function of the heart.

Keywords

Animals, Angiotensin I, Peptide Fragments, Myocardial Reperfusion Injury, Myocytes, Cardiac, Male, Rats, Cardiotonic Agents, Heart Arrest, Induced, Cardioplegic Solutions, L-Lactate Dehydrogenase, Rats, Sprague-Dawley, Rats, Wistar, angiotensin‐(1–7), angiotensin‐(1–9), del Nido cardioplegia, heart, ischemia/reperfusion, myocardial function, renin‐angiotensin system

Published Open-Access

yes

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