Related Experiment Video
Updated: Jul 6, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
[Protective effect of nitric oxide production on myocardium in severely scalded rats]
Ming Zhang1, Yue-sheng Huang, Qiong Zhang
1Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combimed injury, the Third Military Medical University, Chonqing 400038, PR China.
Objective:
To observe the influence of aminoguanidine on cardiac troponin (cTnI) and nitric oxide (NO) levels in serum and myocardium in severely scalded rats.
Methods:
Seventy-two Wistar rats were subjected to 30% TBSA full-thickness scald and randomly divided into scald group(S) and aminoguanidine group (A, with intraperitoneal injection of 40 mg/kg aminoguanidine before scald). The venous blood and myocardial tissue of the rats were harvested for the determination of the level of cTnI and nitrite in both serum and myocardium before scald and at 1, 3, 6, 12 and 24 post-burn hours(PBH). Six sham scalded rats served as control group. The changes in the cTnI level and myocardial function were determined among control group, A and S groups at 6PBH.
Results:
The serum level of NO in S group [(59.6 +/- 5.4) micromol/L] was obviously higher than that before scald [(24.6 +/- 0.8) micromol/L, P < 0.01], and it peaked at 6 PBH, then decreased obviously at 24 PBH, which was still markedly higher than that in A group (P < 0.01). The changes in NO level in myocardium were similar to the above tendency. Compared with S group, the level of cTnI was significantly increased in A group at each time-point. Compared with A group at 6 PBH, the inhibition of the cardiac function was relatively reduced in S group at 6 PBH.
Conclusion:
Inhibition of NO synthesis by aminoguanidine aggravates cardiac damage and impairment of cardiac function of scalded rats, indicating that NO exerts protective effect on myocardium at early stage after a scald injury.
