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. 2010 Jun 11;299(3):H713–H722. doi: 10.1152/ajpheart.00273.2010

Fig. 2.

Fig. 2.

Model of cardiac injury and protection. A: adult Balb/c mice were subjected to 30 min of left anterior descending coronary artery occlusion in the presence or absence of the cardioprotective reagent diethylenetriamine (DETA)/nitric oxide (NO). After 24 h of reperfusion, infarct size was measured by postmortem tetrazolium chloride staining in one cohort of mice, whereas hearts from the other cohort were excised for biochemical analysis. To investigate temporal changes in protein abundance after myocardial ischemia, tissue samples were also harvested after 30 min and 4 h of reperfusion in separate groups. B: infarct size analyses in control and preconditioned mice. Acute myocardial ischemia and reperfusion [occlusion (O) and reperfusion (R)] produced left ventricular infarction, which was significantly reduced by pretreatment with the NO donor DETA/NO. n = 12 mice/group. *P = 0.013.