Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Abstract

Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta. The activities of antioxidant enzymes, concentrations of non-enzymatic antioxidants, and biomarkers of oxidative stress were measured in the LV of aortic-banded animals (LVH), untreated or banded rats subjected to short-term (45 min) atrial pacing [(CTR + S) and (LVH + S), respectively], and untreated (CTR) or sham-operated (SHAM) controls. The results indicate that the increase in heart rate in vivo as a result of atrial pacing to a maximum level, independent of sympathetic nerve activity, leads to a substantial increase in oxidative stress and a marked decline in the activities of antioxidant enzymes in both the normal and hypertrophied left ventricle of the rat. The accompanying increase in tissue content of alpha- and gamma-tocopherols seem to contribute to attenuation of the oxidant stress-related loss of thiol stores in the LV. Stable left ventricular hypertrophy induced by aortic banding for six weeks has a minor impact on the capacity of the endogenous antioxidant defense system in the LV, but significantly and negatively affects the ability of the heart LV to tolerate the stress of tachycardia.

High-Dose Testosterone Propionate Treatment Reverses the Effects of Endurance Training on Myocardial Antioxidant Defenses in Adolescent Male Rats

“…The homogenates were either used immediately for the determination of reduced glutathione (GSH), α- and γ-tocopherols and malondialdehyde (MDA) or spun at 4,000× g (4°C) for 15 min to obtain supernatants for quantification of enzyme activities and protein thiols (-SH). CAT activity and the contents of tocopherols and protein thiols were assessed as described previously [4, 16]. The activities of SOD, GPX and GR, and GSH content were measured using BIOXYTECH kits SOD-525, GPX-340, GR-340, and GSH-400 (OXIS International Inc., Portland, OR, USA) according to the manufacturer’s instructions.…”

“…The excess ROS are disposed of quickly by the cellular antioxidant defense systems consisted of a number of antioxidant enzymes, including (but not limited to) superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC 1.11.1.6), glutathione peroxidase (GPX; EC 1.11.1.9), and glutathione reductase (GR; EC 1.6.4.2), and nonenzymatic antioxidants, such as reduced glutathione (GSH) and α- and γ-tocopherols. Electrically induced tachycardia, which imitates cardiac effects of exercise, acutely decreases the activities of the antioxidant enzymes in the left heart ventricle (LV) in the rat [4], whereas the reports on the effects of exercise training on enzymatic and nonenzymatic antioxidant heart systems are equivocal [5–7]. Notably, there is no data on such effects in adolescents.…”

The effect of resveratrol on angiotensin II levels and the rate of transcription of its receptors in the rat cardiac hypertrophy model

“…At the end of the intervention, in addition to weighing of rats, the cardiac mass was also measured after being washed with cold PBS solution. The serum and heart tissue were collected and kept at -70°C for further studies [12,13].…”

Tropisetron restores normal expression of BAD, SIRT1, SIRT3, and SIRT7 in the rat pressure overload‐induced cardiac hypertrophy model

“…Rats were injected with penicillin (200 kU/kg/day) intramuscularly (IM) for the following 7 days to prevent infection. [ 21,22 ] According to previous studies, cardiac hypertrophy would induce within 2 weeks postoperation. [ 23–25 ]…”