nstantaneous and historical temperature effects on a-pinene
Protective effects of amlodipine on mitochondrial injury
in ischemic reperfused
rat heart
Author Details
Najam Ali Khan
(Corresponding author)
Department
of Pharmacology and Clinical Research, College of Pharmacy, IFTM University,
Moradabad
- 244 001, India
e-mail: alikhan_najam@yahoo.co.in
PronobeshChattopadhyay
Defence Research and Development Organization, Tezpur - 784 001, India
Mohammad
Abid
Department of
Pharmacology and Clinical Research, College of Pharmacy, IFTM University,
Moradabad - 244 001,
India
AbhijeetPawdey
Division of Animal
Surgery, Indian Veterinary Research Institute, Bareilly-243 122, India
KamalKishore
Department of
Pharmacy, M.J.P. Rohilkhand University, Bareilly -
243 006, India
Arun Kumar Wahi
Faculty of Pharmacy,
MIT, Moradabad - 244 001, India
Publication Data
Paper received:
29
September 2010
Revised
received:
05
March 2011
Re-revised
received:
25
April 2011
Re-re-revised
received:
19
May 2011
Accepted:
14 June 2011
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), superoxidedismutase (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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