Abstract
We investigated both the effect of levosimendan and the role of oxidant/antioxidant status and trace element levels in the pulmonary artery of rats. Fourteen male Wistar albino rats were randomly divided into two groups of seven animals each. Group 1 was not exposed to levosimendan and served as a control. Levosimendan (12 μg/kg) diluted in 10 ml 0.9 % NaCl was administered intraperitoneally to group 2. Animals of both groups were killed after 3 days, and their pulmonary arteries were harvested to determine changes in tissue oxidant/antioxidant status and trace element levels. The animals in both groups were killed 72 h after the levosimendan exposure treatment, and pulmonary arteries were harvested to determine levels of the lipid peroxidation product MDA and the antioxidant GSH as well as the decreased activity of antioxidant enzymes such as SOD, GSH-Px and CAT. It was found that MDA levels increased in pulmonary artery tissues of rats after levosimendan administration. The GSH level decreased in the pulmonary artery of rats after levosimendan treatment. Co, Mn, Fe, Cd and Pb levels were significantly higher (P < 0.001) and Mg, Zn and Cu levels significantly lower (P < 0.001) in the levosimendan group compared to the control group. These results suggest that levosimendan treatment caused an increase in free radical production and a decrease in antioxidant enzyme activity in the pulmonary artery of levosimendan-treated rats. It also caused a decrease or increase in the levels of many minerals in the pulmonary artery, which is an undesirable condition for normal pharmacological function.
Highlights
Levosimendan causes venous, arterial and coronary vasodilation, probably by opening ATP-sensitive potassium channels in smooth muscle
This article is published with open access at Springerlink.com. We investigated both the effect of levosimendan and the role of oxidant/antioxidant status and trace element levels in the pulmonary artery of rats
This study was carried out to investigate the effect of intraperitoneal injection of levosimendan on oxidative stress of pulmonary artery in rats
Summary
Levosimendan causes venous, arterial and coronary vasodilation, probably by opening ATP-sensitive potassium channels in smooth muscle. Levosimendan is a cardiovascular drug for the treatment of acute and decompensated heart failure It has positive inotropic and antistunning effects mediated by calcium sensitization of contractile proteins (Pollesello and Papp 2007; Jamali et al 1997) and vasodilatory and anti-ischemic effects mediated by the opening of ATP-sensitive potassium (KATP) channels in vascular smooth muscle cells (Jamali et al 1997; De Witt et al 2002). The superoxide dismutases (SODs) are a major cellular defense system against superoxide in all vascular cells These enzymes contain redox metals in the catalytic center and dismutase superoxide radicals to hydrogen peroxide and oxygen (Wassmann et al 2004). Oxidative stress was measured by the serum levels of MDA, enzymic GPx and SOD as well as trace element levels in the pulmonary artery. With the assumption that levosimendan directed to the pulmonary artery affects adjacent organs in rats, we designed our study to investigate the effect of levosimendan exposure of the pulmonary artery on oxidative stress and some trace element levels in the pulmonary artery
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