Related Experiment Video
Updated: Jul 19, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Renal damage in rats induced by myocardial ischemia/reperfusion: Role of nitric oxide
Hakan Parlakpinar1, Mehmet Kaya Ozer, Ekrem Cicek
1Department of Pharmacology, Inonu University, Malatya, Turkey.
Background:
It has been demonstrated that myocardial ischemia/reperfusion (MI/R) causes renal damage. However, the mechanism underlying this damage in kidneys during revascularization of myocardium is unclear. Direct renal ischemia/reperfusion has been implicated in the induction of inducible nitric oxide synthase (iNOS) that leads to increase production of nitric oxide (NO). Recently, excessive production of NO has been found to be involved in causing renal injury by formatting peroxinitrite (ONOO(-)). The aim of this study was to investigate whether NO has a role in this damage, using aminoguanidine (AMG), a known iNOS inhibitor and an antioxidant, in rats undergoing MI/R.
Methods:
Male Wistar rats were used for the experiments (n = 7 each group). In the MI/R group, the left coronary artery was occluded for 30 min and then reperfused for 120 min; the same procedure was used for the AMG group, with the additional step of AMG (200 mg/kg) administered 10 min prior to ischemia. A control group underwent sham operation. At the end of the reperfusion period, all rats were killed and their kidneys removed for biochemical determination and histopathological analysis.
Results:
Myocardial ischemia/reperfusion in the rat kidney was accompanied by a significant increase in malondialdehyde and NO production, and a decrease in glutathione content. Administration of AMG reduced malondialdehyde and NO production and prevented depletion of glutathione content. These beneficial changes in the biochemical parameters were also associated with parallel changes in histopathological appearance.
Conclusion:
These findings suggest that MI/R plays a causal role in kidney injury and AMG exerts renal-protective effects, probably by inhibiting NO production and antioxidant activities.
Insights
Myocardial ischemia/reperfusion causes kidney damage, but aminoguanidine (AMG) offers renal protection. This study shows AMG reduces nitric oxide (NO) production and oxidative stress, mitigating kidney injury during MI/R.
Area of Science:
- Cardiovascular Research
- Nephrology
- Biochemistry
Background:
- Myocardial ischemia/reperfusion (MI/R) is known to induce renal damage.
- The precise mechanisms linking MI/R to kidney injury remain unclear.
- Increased nitric oxide (NO) production via inducible nitric oxide synthase (iNOS) and subsequent peroxynitrite formation are implicated in renal injury.
Purpose of the Study:
- To investigate the role of NO in kidney damage during MI/R.
- To evaluate the renoprotective effects of aminoguanidine (AMG), an iNOS inhibitor and antioxidant, in a rat model of MI/R.
Main Methods:
- Male Wistar rats underwent MI/R (30 min occlusion, 120 min reperfusion).
- The AMG group received 200 mg/kg AMG 10 minutes prior to ischemia.
- Kidney tissues were analyzed biochemically and histopathologically.
Main Results:
- MI/R significantly increased malondialdehyde and NO production, while decreasing glutathione levels in rat kidneys.
- AMG administration attenuated malondialdehyde and NO increases and prevented glutathione depletion.
- Biochemical improvements correlated with favorable histopathological changes.
Conclusions:
- MI/R plays a direct role in causing kidney injury.
- AMG demonstrates significant renal-protective effects in this model.
- These protective effects are likely mediated by the inhibition of NO production and antioxidant activities of AMG.
