| RESEARCH ARTICLE |
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| Year : 2012 | Volume
: 44
| Issue : 1 | Page : 68-72 |
Evaluation of thyroid hormone induced pharmacological preconditioning on cardiomyocyte protection against ischemic-reperfusion injury
Anil Kumar, Rajeev Taliyan, PL Sharma
Department of Pharmacology, I. S. F. College of Pharmacy, Moga, Punjab, India
Correspondence Address:
Rajeev Taliyan
Department of Pharmacology, I. S. F. College of Pharmacy, Moga, Punjab
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.91870
Objectives: Ischemic preconditioning (IPC) has been demonstrated to make myocardium transiently more resistant to deleterious effect of prolonged ischemia. The opening of the mitochondrial permeability transition pore (mPTP) at the time of myocardial reperfusion is a critical determinant of cell death. L-thyroxine pre-treatment increases the tolerance of the heart to ischemia and produces cardioprotection similar to ischemic precondition. This study has been designed to investigate the mechanism involved in L-thyroxine-induced cardiomyocyte protection against ischemia-reperfusion (I/R) injury in rats.
Materials and Methods: L-thyroxine (T 4 ) was administered to Wistar rats (n=6) (25 μg/100 g/day s.c.) for two weeks. Hearts from normal and L-thyroxine-treated rats were perfused in Langendorff's mode and subjected to 30 min of ischemia followed by 120 min of reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining and lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) was analyzed in coronary effluent.
Results: IPC and pharmacological preconditioning (PPC) significantly decreased (P<0.05) myocardial infarct size, release of LDH and CK-MB in rat heart. Perfusion of atractyloside, an opener of mPTP, significantly (P<0.05) attenuated the cardioprotective effect of IPC and L-thyroxine-induced pharmacological preconditioning (PPC) in normal rat heart.
Conclusion: The cardioprotective effect of L-thyroxine-induced preconditioning may be mediated through inhibition of mPTP opening during reperfusion phase.
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