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Updated: Jun 22, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
[Myocardial infarction remodeling in rats with dinitrosyl iron complex with glutathione]
Insights
Dinitrosyl iron complex with reduced glutathione (DNIC-GS) effectively reduces myocardial infarction size in rats by preserving heart metabolism and membrane integrity. This NO-releasing agent shows promise in limiting heart damage post-ischemia.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Biochemistry
Context:
- Myocardial infarction (MI) remains a leading cause of death globally.
- Effective treatments to limit infarct size and preserve cardiac function are crucial.
- Nitric oxide (NO) releasing agents are being investigated for cardioprotective effects.
Purpose:
- To investigate the effects of dinitrosyl iron complex with reduced glutathione (DNIC-GS) on hemodynamics, cardiac metabolism, and infarct size in a rat model of myocardial infarction.
- To evaluate DNIC-GS as a potential therapeutic agent for limiting ischemic heart damage.
Summary:
- DNIC-GS administration, intravenously before coronary artery occlusion or during reperfusion, significantly reduced myocardial infarction size in rats.
- DNIC-GS demonstrated a vasodilative effect, lowering mean arterial pressure.
- Preischemic DNIC-GS administration reduced plasma levels of cardiac injury markers (LDH, CK-MB) and improved the energy state of the ischemic myocardium without affecting non-ischemic tissue.
Impact:
- DNIC-GS administration promotes cardioprotection by preserving aerobic metabolism and membrane integrity in post-ischemic cardiomyocytes.
- These findings suggest DNIC-GS has therapeutic potential for managing myocardial infarction.
- Further research into NO-releasing compounds like DNIC-GS could lead to novel strategies for treating heart disease.
Abstract:
Effects of dinitrosyl iron complex with reduced glutathione (DNIC-GS) on hemodynamics, metabolic state of the heart and myocardial infarction size were studied in vivo in rats subjected to 40-min occlusion of the anterior descending coronary artery (ADCA) and subsequent 60-min reperfusion. Intravenous bolus injection of DNIC-GS (3.10 or 0.78 micromol/kg body wt) was performed before ADCA occlusion or at the first minute of the reperfusion; the same volume of saline was infused in the control group. Nitroglycerine and nicorandil were used as reference preparations. DNIC-GS administration significantly reduced the mean arterial pressure, thus indicating vasodilative effect of NO releasing. Administration of both doses of DNIC-GS (before ADCA occlusion or at the first minute of the reperfusion) significantly limited the infarction size as compared with that in the control. Preischemic administration of 3.10 micromol DNIC-GS/kg body wt. substantially reduced activities of lactate dehydrogenase and MB-fraction of creatine kinase in blood plasma at the end of the reperfusion compared with these indices in the control. This effect was accompanied with essential improvement of energy state of the area at risk (AR) and with a lack of DNIC-GS influence on metabolism of non-ischemic area of the heart. The obtained results demonstrate that infarction remodelling after intravenous DNIC-GS administration is related to augmented preservation of aerobic metabolism and membrane integrity in post-ischemic cardiomyocytes of the AR.
