Myocardial protection during ischemia-reperfusion by remote preconditioning: a possible role of inducible nitric oxide synthase and glutathione peroxidase | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 14, Volume 26, Issue 2, December 2006, Page 211-227 PDF (226.45 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2006.37556 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
| Sandra Younan* 1; Mary Youssef1; Amal EL-Shehaby2; Eman Obaia2 | ||||
| 1Department of Physiology, Faculty of Medicine, Cairo University | ||||
| 2Department of Medical Biochemistry, Faculty of Medicine, Cairo University | ||||
| Abstract | ||||
| Cardiac ischemia is considered to be one of the deleterious injury increasing the risk of cardiac morbidity and mortality. Remote protection of the heart via ischemiareperfusion of non-vital organs (Remote ischemic preconditioning RIPC) was suggested by many studies as one of the possible cardioprotective intervention. The aim of the present study was to examine the role of inducible nitric oxide synthase (iNOS) and glutathione peroxidase (GPx) in RIPC of the heart prior to ischemiareperfusion injury, and the possibility of protecting cardiac performance and reducing cardiac damage. Four groups of male rabbits (n= 10/group) were included in this study: Control sham operated group (group I); Remote ischemic preconditioning (RIPC) group (group II); ischemia-reperfusion (I/R) group (group III) and RIPC+I/R group (group IV). RIPC was performed in rabbits of group II and IV by repeated four cycles of 10 min each ,of ischemia-reperfusion of femoral artery alternating with intervals of 10 minutes of reperfusion. After 24 hours, groups III and IV were subjected to 30 minutes pre-ischemic perfusion then 30 minutes of left coronary artery occlusion followed by 60 minutes of post-ischemic reperfusion. Serum creatine kinase (CK) was measured and the size of myocardial infarction was estimated at the end of the ischemic phase (as an index of myocardial ischemic injury). Glutathione peroxidase activity and mRNA iNOS expression were assessed in the cardiac tissue of the four groups. RIPC was found to have no significant effect on the left ventricular cardiac performance of normal heart. However, RIPC improved significantly the percentage recovery of the left ventricular developed pressure in group IV following ischemia-reperfusion compared to group III with no significant difference in the percentage recovery of both the contractility index and the heart rate. As regards glutathione peroxidase activity, it was significantly increased in group II compared to group I, and also as a consequence of cardiac ischemia reperfusion, GPx activity was significantly increased in group III compared to group I and II. RIPC and I/R increased significantly the GPx activity in group IV compared to other groups. Moreover, it was found that group IV had a significant increase in cardiac iNOS gene expression compared to group III, associated with a significant improvement of cardiac damage including serum creatine kinase and infraction size. Also, a significant positive correlation was found between GPx activity and iNOS gene expression in group IV. In conclusion, RIPC from skeletal muscles enhanced the recovery of the heart developed pressure, reduced the post-ischemic CK level, reduced the myocardial infarction size and was accompanied by an increase of glutathione peroxidase activity and enhanced iNOS gene expression providing a possible potential target for the development of novel cardioprotective strategies during I/R injury. | ||||
| Keywords | ||||
| Remote preconditioning; glutathione peroxidase; iNOS; and cardiac performance | ||||
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