Beneficial Effects of RNS60 in Cardiac Ischemic Injury

Figures

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  Figure 1. ECG. (a) A. At 3.5 min of hypoxic stress. B. At 9 min of hypoxic stress. (b) STU area in the 9th min of hypoxic stress in ApoE−/−LDLr−/− mice that received the intravenous injection of RNS60 or saline as the control. Values represent mean ± SEM (n = 5); *** p < 0.0001.

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  Figure 2. Changes in biomarkers of hypoxia. (a) Serum troponin T concentration, (b) serum creatine kinase activity in ApoE−/−LDLr−/− mice that received intravenous injection of RNS60 or saline as control 5 h after the hypoxic event. Values represent mean ± SEM (n = 5); * p < 0.02, ** p < 0.006.

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  Figure 3. (a) Left ventricular end-diastolic pressure (LVEDP), (b) left ventricular systolic pressure (LVSP), (c) left ventricular systolic pressure (LVDP), (d) values of dp/dtmax, and (e) values of dp/dtmin- volume relation of the rat heart after 4 h of hypothermic ischemia in the control and the group that received cardioplegia with RNS60. Values represent mean ± SEM (n = 5); * p < 0.01, ** p < 0.05.

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  Figure 4. The release of purine catabolites from the rat heart during the initial 5 min of reperfusion after prolonged hypothermic ischemia in the control and group that received cardioplegia with RNS60. Values represent mean ± SEM (n = 5); * p < 0.02.

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  Figure 5. The myocardial concentration of nucleotide and creatine metabolites in the rat heart at the end of protocol involving 4 h of hypothermic (4 °C) ischemia and 15 min of reperfusion in the control and group that received cardioplegia with RNS60. Values represent mean ± SEM (n = 5); * p < 0.01, ** p < 0.003.