Abstract
The present study was designed to investigate the role of combined administration of Ramipril and Candesartan against in vitro myocardial ischemic reperfusion injury in rat. Male Wistar albino rats were divided into five groups (n = 6) and treated with saline (10 mL/kg), Ramipril (2 mg/kg), Candesartan (1 mg/kg), and the combination of both drugs, respectively 24 h before induction of global ischemia (5 min of stabilization, 9 min of global ischemia, and 12 min of reflow). Combination of Ramipril and Candesartan when compared to the monotherapy significantly increased the levels of superoxide dismutase, reduced glutathione, catalase, and nitric oxide and decreased the levels of thiobarbituric acid reactive substances. In addition, the superior protective role of combination of Ramipril and Candesartan on ischemia induced myocardial damage was further confirmed by well preserved myocardial tissue architecture in light microscopy and transmission electron microscopy analysis studies. The combination was proved to be effective in salvaging the myocardial tissue against ischemic reperfusion injury when compared to the monotherapy of individual drugs and further investigations on protective mechanism of drugs by increasing the nitric oxide level at molecular levels are needed.
Highlights
In spite of the advances in the cardiovascular disease (CVD), ischemic heart disease (IHD) is one of the leading causes of death in the world
Group II: rats treated with saline (10 mL/kg p.o) and subjected to in vitro global ischemia Group III: rats treated with Ramipril (2 mg/kg p.o) and subjected to in vitro global ischemia
Further studies have to be conducted to study these effects to conform further mechanistic changes offered by these drugs. In light of these findings, our study supports the hypothesis that Ramipril and Candesartan have protective role in myocardial ischemic reperfusion injury and justified their use in combination which has significant protective role in the treatment of ischemic heart diseases
Summary
In spite of the advances in the cardiovascular disease (CVD), ischemic heart disease (IHD) is one of the leading causes of death in the world. According to the World Health Organization (WHO), 7,254,000 deaths worldwide (12.8% of all deaths) resulted from IHD in 2008 [1]. Acute myocardial ischemia reperfusion injury (MIRI) is the major cause of the detrimental effects of IHD on the myocardium [2]. MIRI occurs during the invasivetreatments such as, thrombolysis, angioplasty, coronary bypass, and heart transplantation [3]. The treatment for acute myocardial infarction is the use of thrombolytic therapy or primary percutaneous coronary intervention (PCI). These treatments cause myocardial reperfusion injury for which there is no effective therapy [4]
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