alexa Potential Cardioprotective Effects of Orlistat for Treatment of Myocardial Infarction | OMICS International
ISSN: 2572-9462
Journal of Thrombosis and Circulation: Open Access

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Potential Cardioprotective Effects of Orlistat for Treatment of Myocardial Infarction

Francisco Sandro Menezes-Rodrigues1, José Gustavo Padrão Tavares1, Erisvaldo Amarante de Araújo1, Luciana de Paula2, Paolo Ruggero Errante1, Afonso Caricati-Neto1 and Leandro Bueno Bergantin1*

1Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), São Paulo-SP, Brazil

2Laborvisa–Laboratório de Análises Clínicas, São Paulo-SP, Brazil

Corresponding Author:
Leandro Bueno Bergantin, Ph.D
Laboratory of Autonomic and Cardiovascular Pharmacology
Department of Pharmacology-Escola Paulista de Medicina (EPM)
Universida Federal de São Paulo (UNIFESP), Brazil
Tel: 55 11 5576-4973
E-mail: [email protected]

Received Date: July 13, 2017; Accepted Date: July 21, 2017; Published Date: July 28, 2017

Citation: Menezes-Rodrigues FS, Padrão Tavares JG, Araújo EA, Paula LD, Errante PR, et al. (2017) Potential Cardioprotective Effects of Orlistat for Treatment of Myocardial Infarction. J Thrombo Cir 3:e108. doi:10.4172/2572-9462.1000e108

Copyright: © 2017 Bergantin LB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Acute myocardial infarction (AMI) is characterized by ischemic lesions that severely compromise cardiac structure and function, and even the survival of mammals. The ischemic cardiac diseases (ICD) are related to million deaths per year in the world [1,2]. Although convencional therapy is based on the cardiac reperfusion (R), this procedure increases cardiac damage caused by ischemia (I), and severe arrhythmias (e.g. ventricular arrhythmias and atrio-ventricular blockade) [2-5]. Several reports have demonstrated that cardiac arrhythmias caused by myocardial ischemia and reperfusion (I/R) could be originated from bioenergetic, and electrochemical, imbalance triggered mainly by decrease of ATP synthesis by mitochondria, and cytosolic Ca2+ overload in cardiomyocytes [2-5]. This Ca2+ overload is massively worsed by the increase of Ca2+ influx through L-type voltage-activated Ca2+ channels (VACC) caused by continuous membrane depolarization of cardiomyocytes during cardiac I/R [2-5]. In addition, cytosolic Ca2+ overload promotes accumulated Ca2+ in the mitochondrial matrix via increase of Ca2+ influx through mitochondrial uniporter, leading to mitochondrial bioenergetic collapse, and excessive production of free radical, which compromises the structure and function of mitochondria, and other cytoplasmic organelles [2-5]. These cellular mechanisms importantly contribute for developing arrhythmias, and death in AMI patients. Despite continuous advances in AMI treatment, a high ratio of patients dies suddenly in the early hours before arriving at the hospital [6-9]. Most of these early deaths are due to complex ventricular arrhythmias (VA) and atrio-ventricular blockade (AVB) [6-9]. Surprisingly, there is still lack of knowledge about the exact events of these early malignant arrhythmias, and their cellular and molecular mechanisms. Due to involvement of intracellular Ca2+ overload in cardiac arrhythmias caused by myocardial I/R, the use of pharmaceuticals that reduce this Ca2+ overload represents an alternative pharmacological approach to the treatment of ischemic cardiac diseases in humans, including AMI. Nonetheless, the cardiac reperfusion (R) continues to be the therapy more used to treat ICD [6-9]. Among the various risk factors for persuing cardiac I/R, we can highlight obesity; this disease has worldwide importance, and it is intrinsically related to cardiovascular diseases (e.g. atherosclerosis and thrombosis). Therefore, there is an incessant and required worldwide research for drugs that effectively act in the treatment of obesity. This is a metabolic disease that arises from biochemical, hormonal and energetic disorders [10,11]. Several drugs are used for the pharmacotherapy of obesity-FDA approved pharmacological monotherapy options-including orlistat (ORL, pancreatic lipase inhibitor) [12,13]. Therefore, our group decided to evaluate potential cardioprotective effects of the agents used in the pharmacotherapy (such as ORL) of dyslipidemia in normotensive ratstreated with ORL for ten days-and submitted to the model of in vivo cardiac I/R developed by our group [14]. The cardioprotection was analyzed by evaluation of the electrophysiological parameters through the electrocardiogram analysis (arrhythmias), and serum concentration biochemical markers of cardiac lesion produced in response to the cardiac I/R protocol (creatine kinase (CK)), lowdensity lipoprotein cholesterol (LDL-C) and lethality. We observed that the treatment with ORL could decrease the lethality, the serum levels of CK and LDL-C compared to control groups, indicating cardioprotective effects of the ORL. These results suggest that ORL produced cardioprotective effects against cardiac damage caused by cardiac I/R.


Research supported by CNPq, FAPESP and CAPES.


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