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Tacrolimus ameliorates functional disturbances and oxidative stress in isoproterenol-induced myocardial infarction.

Khorrami A, Hammami M, Garjani M, Maleki-Dizaji N, Garjani A - Daru (2014)

Bottom Line: Administration of isoproterenol resulted in myocardial edema and necrosis as well as a marked reduction in the left ventricular systolic pressure (LVSP), left ventricular contractility (LVdP/dtmax) and relaxation (LVdP/dtmin) along with a severe elevation in left ventricular end-diastolic pressure (LVEDP).It was found that all doses of tacrolimus could amend the ECG pattern and ameliorated the isoproterenol induced disturbances in cardiac function.Furthermore, tacrolimus was found to reduce malondialdehyde concentration in serum and myocardium by 50-70% (P < 0.001).

View Article: PubMed Central - PubMed

ABSTRACT

Background: The inflammatory responses play a major role in the pathogenesis of acute myocardial infarction (MI). Early inhibition of inflammation may improve post MI cardiac function. The aim of this study was to investigate the effects of tacrolimus on cardiac function, hemodynamic parameters as well as histopathologic and electrocardiographic changes in isoproterenol-induced myocardial infarction.

Methods: Male Wistar rats were randomly divided into six groups of control, isoproterenol alone, tacrolimus alone, and isoproterenol plus tacrolimus (0.5, 1 and 2 mg/kg). Isoproterenol (100 mg/kg) was injected subcutaneously for two consecutive days to induce myocardial infarction, and simultaneously tacrolimus was administered orally twice a day for three days.

Results and conclusions: Administration of isoproterenol resulted in myocardial edema and necrosis as well as a marked reduction in the left ventricular systolic pressure (LVSP), left ventricular contractility (LVdP/dtmax) and relaxation (LVdP/dtmin) along with a severe elevation in left ventricular end-diastolic pressure (LVEDP). Isoproterenol also elevated the ST-segment and suppressed the R-amplitude and R-R interval on ECG. It was found that all doses of tacrolimus could amend the ECG pattern and ameliorated the isoproterenol induced disturbances in cardiac function. Acute and short term treatment with tacrolimus at dose of 2 mg/kg significantly (P < 0.001) improved LVdP/dtmax from 2712 ± 82 in myocardial infarcted rats to 4592 ± 149 mmHg/sec. Similarly, tacrolimus lowered LVEDP from 17.6 ± 0.68 in MI group to the value of 5.6 ± 0.22 mmHg (P < 0.001). Furthermore, tacrolimus was found to reduce malondialdehyde concentration in serum and myocardium by 50-70% (P < 0.001).

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Effect of tacrolimus on electrocardiographic patterns and changes (recorded from limb lead II) in normal control, tacrolimus alone treated group (Sham), isoproterenol alone injected (ISO), and rats treated with tacrolimus (Tac: 0.5, 1, 2 mg/kg).
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Fig1: Effect of tacrolimus on electrocardiographic patterns and changes (recorded from limb lead II) in normal control, tacrolimus alone treated group (Sham), isoproterenol alone injected (ISO), and rats treated with tacrolimus (Tac: 0.5, 1, 2 mg/kg).

Mentions: The Lead II electrocardiograms obtained from animals were shown in Figure 1. The rats were received tacrolimus alone (sham) showed normal patterns of ECG, while the rats treated with isoproterenol alone (MI group) demonstrated significant changes in ECG pattern. The changes included a marked elevation of ST segment from 95 ± 5.2 μv in control group to 194 ± 14.2 μv in ISO-treated group (P < 0.001), and a reduction in R wave amplitude from 448 ± 27 μv in control group to 267 ± 15 μv in ISO-treated group (P < 0.001) which both are indicative of myocardial infarction (Figure 2). Oral treatment with tacrolimus at doses of 0.5, 1 and 2 mg/kg significantly suppressed the isoproterenol-induced ST-segment elevation from 194 ± 14.2 μv in ISO-treated group to 169 ± 12.7, 113 ± 8.4 and 121 ± 11 μv in tacrolimus-treated groups, respectively.Figure 1


Tacrolimus ameliorates functional disturbances and oxidative stress in isoproterenol-induced myocardial infarction.

Khorrami A, Hammami M, Garjani M, Maleki-Dizaji N, Garjani A - Daru (2014)

Effect of tacrolimus on electrocardiographic patterns and changes (recorded from limb lead II) in normal control, tacrolimus alone treated group (Sham), isoproterenol alone injected (ISO), and rats treated with tacrolimus (Tac: 0.5, 1, 2 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4201681&req=5

Fig1: Effect of tacrolimus on electrocardiographic patterns and changes (recorded from limb lead II) in normal control, tacrolimus alone treated group (Sham), isoproterenol alone injected (ISO), and rats treated with tacrolimus (Tac: 0.5, 1, 2 mg/kg).
Mentions: The Lead II electrocardiograms obtained from animals were shown in Figure 1. The rats were received tacrolimus alone (sham) showed normal patterns of ECG, while the rats treated with isoproterenol alone (MI group) demonstrated significant changes in ECG pattern. The changes included a marked elevation of ST segment from 95 ± 5.2 μv in control group to 194 ± 14.2 μv in ISO-treated group (P < 0.001), and a reduction in R wave amplitude from 448 ± 27 μv in control group to 267 ± 15 μv in ISO-treated group (P < 0.001) which both are indicative of myocardial infarction (Figure 2). Oral treatment with tacrolimus at doses of 0.5, 1 and 2 mg/kg significantly suppressed the isoproterenol-induced ST-segment elevation from 194 ± 14.2 μv in ISO-treated group to 169 ± 12.7, 113 ± 8.4 and 121 ± 11 μv in tacrolimus-treated groups, respectively.Figure 1

Bottom Line: Administration of isoproterenol resulted in myocardial edema and necrosis as well as a marked reduction in the left ventricular systolic pressure (LVSP), left ventricular contractility (LVdP/dtmax) and relaxation (LVdP/dtmin) along with a severe elevation in left ventricular end-diastolic pressure (LVEDP).It was found that all doses of tacrolimus could amend the ECG pattern and ameliorated the isoproterenol induced disturbances in cardiac function.Furthermore, tacrolimus was found to reduce malondialdehyde concentration in serum and myocardium by 50-70% (P < 0.001).

View Article: PubMed Central - PubMed

ABSTRACT

Background: The inflammatory responses play a major role in the pathogenesis of acute myocardial infarction (MI). Early inhibition of inflammation may improve post MI cardiac function. The aim of this study was to investigate the effects of tacrolimus on cardiac function, hemodynamic parameters as well as histopathologic and electrocardiographic changes in isoproterenol-induced myocardial infarction.

Methods: Male Wistar rats were randomly divided into six groups of control, isoproterenol alone, tacrolimus alone, and isoproterenol plus tacrolimus (0.5, 1 and 2 mg/kg). Isoproterenol (100 mg/kg) was injected subcutaneously for two consecutive days to induce myocardial infarction, and simultaneously tacrolimus was administered orally twice a day for three days.

Results and conclusions: Administration of isoproterenol resulted in myocardial edema and necrosis as well as a marked reduction in the left ventricular systolic pressure (LVSP), left ventricular contractility (LVdP/dtmax) and relaxation (LVdP/dtmin) along with a severe elevation in left ventricular end-diastolic pressure (LVEDP). Isoproterenol also elevated the ST-segment and suppressed the R-amplitude and R-R interval on ECG. It was found that all doses of tacrolimus could amend the ECG pattern and ameliorated the isoproterenol induced disturbances in cardiac function. Acute and short term treatment with tacrolimus at dose of 2 mg/kg significantly (P < 0.001) improved LVdP/dtmax from 2712 ± 82 in myocardial infarcted rats to 4592 ± 149 mmHg/sec. Similarly, tacrolimus lowered LVEDP from 17.6 ± 0.68 in MI group to the value of 5.6 ± 0.22 mmHg (P < 0.001). Furthermore, tacrolimus was found to reduce malondialdehyde concentration in serum and myocardium by 50-70% (P < 0.001).

Show MeSH
Related in: MedlinePlus