Protective effects of amlodipine on mitochondrial injury in ischemic reperfused rat heart.
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Date
2012-05
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Abstract
The most significant finding of the present study was the release of nitric oxide (NO). The effect of amlodipine
on NO production associated with ischemic reperfused (IR) injury was investigated in rat heart model.
Cardiac tissues from animal groups were processed for biochemical, histopathological and electron microscopic
studies. There was a significant increase in myocardial catalase (CAT), superoxide dismutase (SOD) and
glutathione (GSH) enzymes in amlodipine treated group (1.37, 10.27, 6.39) when compared to IR injured
group (0.81, 6.87, 4.53). Histopathology studies showed amlodipine reduce cardiocyte damage in cardiac
injury during the cardiac IR. Transmission electron microscopic (TEM) study confirmed the cardioprotective
role of amlodipine against IR induced cardiac injury. On the basis of findings, it is hypothesized that a portion
of the beneficial actions of amlodipine may involve the release or action of NO and probably by its antioxidant
properties.
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Keywords
Ischemic-reperfusion injury, Amlodipine, Reactive oxygen species
Citation
Khan Najam Ali, Chattopadhyay Pronobesh, Abid Mohammad, Pawdey Abhijeet, Kishore Kamal, Wahi Arun Kumar. Protective effects of amlodipine on mitochondrial injury in ischemic reperfused rat heart. Journal of Environmental Biology. 2012 May; 33(3): 591-595.