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Published on: April 26, 2015
Protective Effect of Cilostazol Against Restraint Stress Induced Heart Failure in Post-Myocardial Infarction Rat
Moon Young Lee1, Nam Ho Kim2, Jum Suk Ko2
1Department of Physiology and Institute of Wonkwang Medical Science, Wonkwang University School of Medicine, Iksan, Korea.
Insights
Cilostazol treatment improved heart function and reduced harmful remodeling in post-heart attack rats subjected to stress. These benefits were linked to lower stress hormone levels after myocardial infarction (MI).
Area of Science:
- Cardiovascular Pharmacology
- Myocardial Infarction Research
- Stress Physiology
Background:
- Cilostazol, a phosphodiesterase III inhibitor, possesses antiplatelet and vasodilatory properties.
- It exhibits pleiotropic effects, including antioxidant and calcium modulation.
- Myocardial infarction (MI) and associated stress can lead to adverse cardiac remodeling and dysfunction.
Purpose of the Study:
- To investigate the in vivo effects of cilostazol on myocardial function, remodeling, and neurohormonal status in a rat model of myocardial infarction with restraint stress.
- To assess cilostazol's impact on left ventricular ejection fraction (LVEF), cardiac mass, and stress-related biomarkers.
Main Methods:
- Male Sprague Dawley rats underwent coronary artery ligation to induce myocardial infarction (MI).
- Rats received either standard chow or cilostazol (5 mg/kg for 5 weeks) and were subjected to restraint stress.
- Left ventricular ejection fraction (LVEF), heart weight/body weight ratio (LV mass), tissue brain natriuretic peptide (BNP), and plasma catecholamine levels were measured.
Main Results:
- Cilostazol treatment significantly increased mean LVEF compared to controls at 5 weeks post-MI (66.9% vs 47.0%).
- LV mass and tissue BNP expression were significantly reduced in the cilostazol group.
- Plasma epinephrine and norepinephrine levels were also significantly lower in rats treated with cilostazol.
Conclusions:
- Cilostazol effectively preserves left ventricular systolic function in post-MI rats under stress conditions.
- Cilostazol treatment attenuates stress-induced cardiac remodeling and reduces adverse neurohormonal activation.
- The beneficial effects of cilostazol are associated with decreased plasma catecholamine levels during post-MI remodeling.
Abstract:
Cilostazol, a phosphodiesterase III inhibitor, has antiplatelet and vasodilatory effects. It also has pleiotrophic effects including reduction of oxygen free radicals, positive chronotropic effect and inhibition of intracellular Ca2+ associated catecholamine secretion. The study was aimed to examine, in vivo, the effects of cilostazol treatments on myocardial function, myocardial remodeling, and neurohormonal status in myocardial infarction (MI) with restrained stress rat model. Male Sprague Dawley rats, subjected to coronary artery ligation to induce myocardial infarction (MI), received either a standard rat chow alone (control, n=5) or combined with cilostazol (cilostazol, n=5; 5 mg/kg×5 weeks). They were exposed to repeated restraint stress (2 h×2 times/day) for 10 days beginning 1 week after surgery. Left ventricular ejection fraction (LVEF), LV mass by heart weight/body weight ratio and level of tissue brain natriuretic peptide (BNP) expression by immunoblotting were determined. Plasma epinephrine and norepinephrine levels were also measured. Mean LVEF was higher in the cilostazol group than in the control group (66.9±14.3 vs 47.0±17.1, p<0.05) at 5 weeks after MI. However, LV mass and tissue BNP expression were significantly lower in the cilostazol than in the control group (p<0.05). Plasma epinephrine and norepinephrine levels were also lower in the cilostazol group compared with the control (p<0.05). Cilostazol preserves left ventricular systolic function and attenuates stress induced remodeling in postinfarct rats. Its beneficial effects were associated with reduced plasma catecholamine levels during postinfarct remodeling.
