Myocardial salvaging effect of telmisartan in experimental model of myocardial infarction

Goyal, Sameer N.; Arora, Sachin; Mittal, Rajan; Joshi, Sujata; Nag, Tapas Chandra; Ray, Ruma; Kumari, Santosh; Arya, Dharamvir Singh

doi:10.1016/j.ejphar.2009.07.026

Cited by 29 publications

(30 citation statements)

References 62 publications

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“…In addition to this, Akila and colleagues [Akila et al 2007] showed significant increases in catalase activity after reperfusion, suggesting that the antioxidant defence system protects the cells against reactive species. Administration of telmisartan and olmesartan reduces this increased level of malondialdehyde (Table 1) [Goyal et al 2009;Zhang et al 2007]. The occurrence of oxidative stress in the ISOinjected rats was indicated by the increase of cardiac malondialdehyde content.…”

Section: Antioxidative Agentsmentioning

confidence: 99%

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Garg

Kumari

2014

Therapeutic Advances in Cardiovascular Disease

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High incidences of myocardial infarction associated with high morbidity and mortality, are a major concern and economic burden on industrialized nations. Persistent β-adrenergic receptor stimulation with isoproterenol leads to the development of oxidative stress, myocardial inflammation, thrombosis, platelet aggregation and calcium overload, which ultimately cause myocardial infarction. Therapeutic agents that are presently employed for the prevention and management of myocardial infarction are beta-blockers, antithrombotics, thrombolytics, statins, angiotensin converting enzyme inhibitors, angiotensin II type 1 receptor blockers, calcium channel blockers and nitrovasodilators. In spite of effective available interventions, the mortality rate of myocardial infarction is progressively increasing. Thus, there has been a regular need to develop effective therapies for the prevention and management of this insidious disease. In this review, the authors give an overview of the consequences of isoproterenol in the pathogenesis of cardiac disorders and various therapeutic possibilities to prevent these disorders.

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Section: Antioxidative Agentsmentioning

confidence: 99%

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Garg

Kumari

2014

Therapeutic Advances in Cardiovascular Disease

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“…Our demonstration that PPAR-γ activity was necessary for Telm-induced reversal of Iso-induced decreases in adiponectin [29] , suggesting that Telm exerts its protective effects against Iso-induced cardiac injury in vivo in two ways, functioning as an ARB as well as a PPAR-γ activator. Moreover, activated PPAR-γ, which has anti-infl ammatory and antioxidant effects [30] , has been shown to stimulate adiponectin expression in adipocytes and to upregulate adiponectin plasma levels in animals and humans [31,32] .…”

Section: Discussionmentioning

confidence: 92%

Telmisartan attenuates isoproterenol-induced cardiac remodeling in rats via regulation of cardiac adiponectin expression

Guo

Han

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate whether telmisartan (Telm) pretreatment attenuates isoproterenol (Iso)-induced postinfarction remodeling (PIR) in rats, and whether the effect of Telm is associated with cardiac expression of adiponectin. Methods: PIR was induced in male Wistar rats with two consecutive injections of Iso (80 mg/kg, sc) at an interval of 24 h. Primary culture of ventricular myocytes from neonatal rats was prepared. Iso-induced cardiomyocyte injury was assessed based on cell growth and lactate dehydrogenase (LDH) activity. Cardiac adiponectin expression was measured using qRT-PCR and immunoblot analysis. , po for 65 d) suppressed Iso-induced increases in gravimetric parameters, cardiomyocyte diameter and collagen volume fraction, but had no effect on Iso-induced myocardial hypertrophy and interstitial fi brosis. The protective effect of Telm was associated with enhanced protein expression of cardiac adiponectin. In cultured cardiomyocytes, Telm (5-20 μmol/L) inhibited the cell death and LDH release induced by Iso (10 μmol/L), and reversed Iso-induced reduction in adiponectin protein expression. In cardiomyocytes exposed to Iso (20 μmol/L), GW9662 (30 μmol/L), a selective antagonist of PPAR-γ, blocked the effects of Telm pretreatment on adiponectin protein expression, as well as the protective effects of Telm on Iso-induced cell injury. Conclusion: Telm attenuates Iso-induced cardiac remodeling and cell injury, which is associated with induction of cardiac adiponectin expression.

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“…After recording the hemodynamic parameters, animals of all groups were killed with an overdose of anesthesia (sodium pentobarbitone 100 mg/kg, i.v.) and their hearts were excised and processed for biochemical, histopathological, and ultrastructural studies [13].…”

Section: Surgical Procedures For Evaluating Hemodynamic Parametersmentioning

confidence: 99%

“…The specimens were then washed in phosphate buffer, dehydrated with graded acetone, and then embedded in araldite CY212 to make tissue blocks. Sections (70-80 nm) were cut by ultramicrotome (Ultracut E, Reichert, Austria) and stained with uranyl acetate and lead acetate, and examined under transmission electron microscope (Morgagni 268 D, Fei Co., The Netherlands) by a morphologist blinded to the treatment protocol [13].…”

Section: Transmission Electron Microscopic Studymentioning

confidence: 99%

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Valsartan, an Angiotensin II Receptor Blocker, Attenuates Cardiac Dysfunction and Oxidative Stress in Isoproterenol-Induced Cardiotoxicity

et al. 2011

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Valsartan has significant blood pressure lowering effect via modulating renin-angiotensin system although its mechanism of action in isoproterenol (ISO)-induced myocardial injury is largely unknown. We therefore evaluated the effect of valsartan in ISO-induced oxidative stress and cardiotoxicity during β-adrenergic receptor stimulation in rats. ISO (85 mg/kg, s.c.) was administered on thirteenth and fourteenth day for induction of cardiotoxicity. ISO-treated rats showed significant decrease (P < 0.01) in mean arterial pressure (70.2 ± 9.11 vs. 104.86 ± 8.93), maximal positive (1601.3 ± 338.87 vs. 2789.16 ± 301.76), and negative (1495.76 ± 151.78 vs. 2039.6 ± 279.1) rate of developed left ventricular pressure and increase in left ventricular end-diastolic pressure (5.81 ± 0.51 vs. 2.37 ± 0.43) as compared to the sham group. Similarly, significant reduction in CK-MB (91.42 ± 5.88 vs. 142.63 ± 6.9), LDH (50.52 ± 5.18 vs. 73.28 ± 4.29) levels, and anti-oxidant enzymes activities were observed. Valsartan (15, 30, and 60 mg/kg/day, p.o.) pretreatment for 14 days favorably modulated these altered parameters. However, valsartan (60 mg/kg) only showed significant improvement (P < 0.01) in cardiac dysfunction, myocardial injury markers, and anti-oxidant status of myocardium in ISO-induced cardiotoxicity. Histopathology and ultrastructural studies further validated the protective effect of valsartan (60 mg/kg). Altogether, these results suggest that cardioprotective effect of valsartan is mediated through augmenting endogenous anti-oxidant defense system, preserving hemodynamic function and structural integrity of myocardium.

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Myocardial salvaging effect of telmisartan in experimental model of myocardial infarction

Cited by 29 publications

References 62 publications

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Telmisartan attenuates isoproterenol-induced cardiac remodeling in rats via regulation of cardiac adiponectin expression

Valsartan, an Angiotensin II Receptor Blocker, Attenuates Cardiac Dysfunction and Oxidative Stress in Isoproterenol-Induced Cardiotoxicity

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