2012The Journal of Clinical AnesthesiologyRequires access

The protection of hydrogen sulfide delayed preconditioning in rat myocardium after ischemic reperfusion

Chang Ye-tia

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Abstract

Objective To investigate the protection of hydrogen sulfide delayed preconditioning on myocardial ischemia reperfusion injury in rats.Methods Thirty Sprague-Dawley male rats were assigned randomly into three groups (n=10 each): group S, control rats that received sham operation; group IR, rats treated with NS (1.0 ml/kg iv) 24 h before ischemia; and group H, rats treated with NaHS (0.05 mg/kg iv) 24 h before ischemia. Group IR and H were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS), the activity of superoxide dismutase(SOD) and the content of malondialdehyde (MDA) in blood were measured. The myocardial ultrastructures were observed under the electron microscopy.Results The IS was significantly reduced in group H (25.40±3.54)% as compared with group IR(38.27±5.64)% (P0.05). Group H had a lower level of MDA and a higher level of SOD than that of group IR (P0.05). The degree injury of group H was change better than that of group IR under the electron microscope.Conclusion Hydrogen sulfide delayed preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats by anti-oxidant reaction.

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Objective To investigate the protection of hydrogen sulfide delayed preconditioning on myocardial ischemia reperfusion injury in rats.Methods Thirty Sprague-Dawley male rats were assigned randomly into three groups (n=10 each): group S, control rats that received sham operation; group IR, rats treated with NS (1.0 ml/kg iv) 24 h before ischemia; and group H, rats treated with NaHS (0.05 mg/kg iv) 24 h before ischemia. Group IR and H were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS), the activity of superoxide dismutase(SOD) and the content of malondialdehyde (MDA) in blood were measured. The myocardial ultrastructures were observed under the electron microscopy.Results The IS was significantly reduced in group H (25.40±3.54)% as compared with group IR(38.27±5.64)% (P0.05). Group H had a lower level of MDA and a higher level of SOD than that of group IR (P0.05). The degree injury of group H was change better than that of group IR under the electron microscope.Conclusion Hydrogen sulfide delayed preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats by anti-oxidant reaction.

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Available abstract

Objective To investigate the protection of hydrogen sulfide delayed preconditioning on myocardial ischemia reperfusion injury in rats.Methods Thirty Sprague-Dawley male rats were assigned randomly into three groups (n=10 each): group S, control rats that received sham operation; group IR, rats treated with NS (1.0 ml/kg iv) 24 h before ischemia; and group H, rats treated with NaHS (0.05 mg/kg iv) 24 h before ischemia. Group IR and H were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS), the activity of superoxide dismutase(SOD) and the content of malondialdehyde (MDA) in blood were measured. The myocardial ultrastructures were observed under the electron microscopy.Results The IS was significantly reduced in group H (25.40±3.54)% as compared with group IR(38.27±5.64)% (P0.05). Group H had a lower level of MDA and a higher level of SOD than that of group IR (P0.05). The degree injury of group H was change better than that of group IR under the electron microscope.Conclusion Hydrogen sulfide delayed preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats by anti-oxidant reaction.

Key concepts: Medicine, Malondialdehyde, Cardioprotection, Ischemia, Hydrogen sulfide, Superoxide dismutase, Reperfusion injury, Anesthesia

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