TY - JOUR
T1 - Cardioprotective response to chronic administration of vitamin E in isoproterenol induced myocardial necrosis
T2 - Hemodynamic, biochemical and ultrastructural studies
AU - Nandave, Mukesh
AU - Mohanty, Ipseeta
AU - Nag, T. C.
AU - Ojha, Shreesh Kumar
AU - Mittal, Rajan
AU - Kumari, Santosh
AU - Arya, Dharamvir Singh
N1 - Funding Information:
We are grateful to University Grant Commission (UGC) for providing financial assistance. The authors are also thankful to Electron Microscopy Facility, All India Institute of Medical Science, New Delhi.
PY - 2007
Y1 - 2007
N2 - The present study evaluated the cardioprotective potential of vitamin-E by studying its effect on hemodynamic parameters, lipid peroxidation, myocyte injury marker and ultrastructural changes in model of isoproterenol-induced myocardial necrosis in rats. Wistar albino male rats (150-200 g) were randomly divided into saline, ISP control, and vit E groups. Vitamin E group was administered vitamin E at a dose of 100 mg/kg/day while saline and ISP control groups received saline orally for one month. On 29th and 30 th day, ISP (85 mg/kg, sc) was administered at an interval of 24 h to vit E and ISP control rats. On 31st day, rats of all groups were anesthetized and hemodynamic parameters were recorded. At the end of experimentation, animals were sacrificed; hearts were excised and processed for biochemical and ultrastructural studies. ISP administration produced marked cardiac necrosis as evidenced by significant decrease in myocardial creatine kinase- MB as well as increase in malonaldialdehyde levels. ISP-induced myocardial necrosis resulted in myocardial dysfunction as evidenced by significant depression in heart rate and mean arterial pressure in the ISP control group as compared to saline control. Salient ultrastructural changes including extensive loss of myofibrils, muscle necrosis, loss of mitochondria, and formation of several intracytoplasmic vacuoles and lipid droplets further confirmed the ISP-induced myocardial damage. However, subsequent to ISP challenge, vit E treatment significantly preserved the myocardium by restoring myocardial CK-MB activity, inhibiting the ISP-induced lipid peroxidation and ultrastructural changes. Additionally, pre-and co-treatment of vit E prevented the deleterious ultrastructural changes caused by ISP. These beneficial effects of chronic vit E treatment also translated into significant restoration of the altered hemodynamic parameters. The present study clearly demonstrated the cardioprotective potential of vit E at dose of 100 mg/kg in ISP-induced model of myocardial necrosis in rats. The significant restoration of altered hemodynamic parameters, myocardial CK-MB activity, prevention of ISP-induced rise in lipid peroxidation and ultrastructural changes may confirm its cardioprotective effect.
AB - The present study evaluated the cardioprotective potential of vitamin-E by studying its effect on hemodynamic parameters, lipid peroxidation, myocyte injury marker and ultrastructural changes in model of isoproterenol-induced myocardial necrosis in rats. Wistar albino male rats (150-200 g) were randomly divided into saline, ISP control, and vit E groups. Vitamin E group was administered vitamin E at a dose of 100 mg/kg/day while saline and ISP control groups received saline orally for one month. On 29th and 30 th day, ISP (85 mg/kg, sc) was administered at an interval of 24 h to vit E and ISP control rats. On 31st day, rats of all groups were anesthetized and hemodynamic parameters were recorded. At the end of experimentation, animals were sacrificed; hearts were excised and processed for biochemical and ultrastructural studies. ISP administration produced marked cardiac necrosis as evidenced by significant decrease in myocardial creatine kinase- MB as well as increase in malonaldialdehyde levels. ISP-induced myocardial necrosis resulted in myocardial dysfunction as evidenced by significant depression in heart rate and mean arterial pressure in the ISP control group as compared to saline control. Salient ultrastructural changes including extensive loss of myofibrils, muscle necrosis, loss of mitochondria, and formation of several intracytoplasmic vacuoles and lipid droplets further confirmed the ISP-induced myocardial damage. However, subsequent to ISP challenge, vit E treatment significantly preserved the myocardium by restoring myocardial CK-MB activity, inhibiting the ISP-induced lipid peroxidation and ultrastructural changes. Additionally, pre-and co-treatment of vit E prevented the deleterious ultrastructural changes caused by ISP. These beneficial effects of chronic vit E treatment also translated into significant restoration of the altered hemodynamic parameters. The present study clearly demonstrated the cardioprotective potential of vit E at dose of 100 mg/kg in ISP-induced model of myocardial necrosis in rats. The significant restoration of altered hemodynamic parameters, myocardial CK-MB activity, prevention of ISP-induced rise in lipid peroxidation and ultrastructural changes may confirm its cardioprotective effect.
KW - Isoproterenol
KW - Myocardial necrosis
KW - Rats
KW - Vitamin E
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U2 - 10.1007/BF02912876
DO - 10.1007/BF02912876
M3 - Article
C2 - 23105647
AN - SCOPUS:33947148573
SN - 0970-1915
VL - 22
SP - 22
EP - 28
JO - Indian Journal of Clinical Biochemistry
JF - Indian Journal of Clinical Biochemistry
IS - 1
ER -