Modulation of ECG, Myocardial Oxidative Stress Markers and Connexion 43 Expression by Ascorbic Acid and Ferulic Acid in Isoproterenol-Induced Myocardial Infarction in Rats

Metias, Emile F; Abo-Elmaaty, Nisreen; Hussein, Abdelaziz M.; Abdallah, Eman W; Abdel-Aziz, Azza

doi:10.4172/2168-9652.1000210

Cited by 17 publications

(18 citation statements)

References 35 publications

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“…The symbol "*" denotes significant versus NC group, "#" denotes significant versus Ali group, and "$" denotes significant versus ISO group NC: normal control; ISO: isoproterenol; Ali: aliskiren; Group A: no histopathological changes; Group B: mild histopathological changes; Group C: moderate and/or severe histopathological changes studied parameters, whereas inhibition of RAS in normal rats did not cause any significant change in the studied parameters. In this study, we confirmed previous findings that showed a significant rise in serum levels of LDH and CK-MB in the ISO group, which was expected as a consequence of destruction of myocardial cell membranes by ISO (12,41,46). In Recently, Khan et al (30) reported that administration of ISO (85 mg/kg) in two doses with 24-h intervals in rats caused a significant increase in markers of cardiac injury (LDH and CK-MB) with significant reduction in ABP, maximum rate of development of left ventricular (LV) pressure, and increase in LV end diastolic pressure.…”

Section: Discussionsupporting

confidence: 92%

“…Specimens of myocardium from the NC group showing normal architecture of rat myocardium at 200× (a) and 400× (b), from the Ali group showing normal architecture of rat myocardium at 200× (c) and 400× (d), from the ISO group, area of infarction with interstitial edema with marked neutrophil infiltration at 400× (e-g), and from the Ali + ISO group, area of infarction with marked interstitial edema with acute extensive myofibrillary degeneration and hemorrhage (h), severe interstitial edema with marked neutrophil infiltration and moderate myofibrillary degeneration (i), and interstitial edema with interstitial hemorrhage (j) (H&E, 400×) consistence with functional abnormalities of cardiac functions, histopathological examination of cardiac tissues obtained from the ISO-MI group showed the characteristic findings of MI. These findings are similar to those reported by Dhalla et al(12) and Metias et al(41).…”

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confidence: 93%

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Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

et al. 2018

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This study examined the effects of aliskiren (Ali) (direct renin inhibitor) on serum cardiac enzymes (LDH and CK-MB), electrocardiography (ECG) changes, myocardial oxidative stress markers (MDA, CAT, and GSH) and the expression of Bcl2, HO-1, and Nrf2 genes in isoproterenol (ISO)-induced myocardial infarction (MI). A total of 40 male albino rats were allocated into four groups, (1) normal control (NC) group, (2) Ali group (rats received Ali at 10 mg/kg/day p.o. for 5 days), (3) ISO group (rats received ISO 150 mg/kg i.p. for two consecutive days at 24 h intervals), and (4) Ali + ISO group (rats received ISO + Ali at 10 mg/kg/day p.o. for 5 days from the 2 dose of ISO). ISO group showed significant rise in serum cardiac enzymes (CK-MB and LDH), myocardial damage scores, myocardial MDA, HO-1, myocardial Nrf2 expression with significant reduction in myocardial antioxidants (CAT and GSH), and Bcl2 expression compared to the normal group (p < 0.05). ECG showed ST segment elevation, prolonged QT interval and QRS complex, and increased heart rate in ISO group. Co-administration of Ali and ISO caused significant increase in cardiac enzymes and morphology with increase in MDA, serum K, and creatinine with significant decrease in Bcl2, HO-1, and Nrf2 without significant changes in ECG parameters compared to ISO group. We concluded that low dose of Ali seems to exacerbate the myocardial injury in ISO-MI, which might be due to the enhanced oxidative stress and apoptosis.

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Section: Discussionsupporting

confidence: 92%

supporting

confidence: 93%

Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

et al. 2018

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“…Further, it has been demonstrated that an increase in heart rate is responsible for increased oxygen consumption leading to accelerated myocardial necrosis. 28 Our finding also indicate increase in HR in ISOcontrol animals the increase in probably causes cardiac dysfunction and contractile failure in heart. The QRS complex shows total duration of ventricular depolarization.…”

Section: Discussionsupporting

confidence: 65%

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Shikalgar¹,

Naikwade²

2018

Int. Res. J. Pharm.

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The aim of study was to evaluate cardio protective activity of fulvic acid in Isoprenaline induced cardiac toxicity. In current investigation, female/male wistar rats were divided into five groups, normal, control, Fulvic acid 100mg/kg, Fulvic acid 200mg/kg, and Fulvic acid 300 mg/kg. Isoprenaline 85 mg/kg was administered on 29 th and 30 th day during study period to all except normal group. Fulvic acid was administered to respective groups once daily for total 30 days, on the last day of study, the animals were anesthetized to record ECG and BP (by cannulating carotid artery), blood was collected from carotid artery and SGOT, LDH And CK-MB were estimated, Animals were sacrificed to isolate heart and preparation of tissue homogenate. The antioxidant status is analyzed by measuring MDA content, SOD CAT, GSH activity. The tissue sample is also preserved for histological studies. Isoprenaline causes cardiac damage which was manifested by alteration in serum cardiac markers, antioxidant markers, ECG and hemodynamic and histological changes. These alterations were restored due to treatment with fulvic acid 300mg/kg. With data obtained in study it have been concluded that fulvic acid treatment for 4 weeks protect the heart of rat from cardiotoxicity as a result of isoprenaline administration.

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“…Worldwide, cardiovascular diseases are the main cause of death in the occidental lifestyle [1]. In the countries of America, 75% of deaths are associated with heart diseases [2,3].…”

Section: Introductionmentioning

confidence: 99%

Metabolic Disorders Cardiac: Disturbances Triggers by Lack of ATP?

Ob¹

2018

Biochem Anal Biochem

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Occidental lifestyle including lack of physical activity, are related to risk of developing heart diseases. ATP has a central role in understanding cardiac metabolism. Thus, this study was carried out to discuss aerobic cardiac metabolism, with most of the energy provided by oxidative phosphorylation. The ATP produced by this pathway is essentially used for contraction in non-pathological conditions. In addition, situations are discussed on the glycolytic pathway to produce ATP under pathological conditions. Thus, in some cardiomyopathies, the manipulation of the metabolic status of the heart represents an attractive alternative for the prevention of later complications.

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Modulation of ECG, Myocardial Oxidative Stress Markers and Connexion 43 Expression by Ascorbic Acid and Ferulic Acid in Isoproterenol-Induced Myocardial Infarction in Rats

Cited by 17 publications

References 35 publications

Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Metabolic Disorders Cardiac: Disturbances Triggers by Lack of ATP?

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