Abstract
Cardiovascular diseases are the principal cause of decease in the world, 16.4% of the worldwide population dies every year as consequence of myocardial infarction (MI) (WHO, 2013).In the myocardium infarction a vascular occlusion originates isquemic necrosis and decrease of coronary flow. Several models had been developed to research this pathology, nonetheless not all models offer the possibility to evaluate each stage of MI, which limits the understanding of this phenomena. In 1956, Rona found that isoproterenol (ISO), a beta adrenergic agonist, is able to i nduce MI in rats. This model, characterized biochemical , histological and physiologically (Chagoya, 1997) allows the study of every stage of MI: pre- infarction, infarction (12 hours after ISO administration) and post-infarction. Correct inflammatory responses during the post infarction phase leads to the formation of a scar with enough force to prevent the extension of the infarct, which is necessary for an accurate h ealing process (Anzai, 2013).It has been reported that adenosine has a strong role in the inflammation process.(Haskó, 2004). In previous studies achieved in our laboratory it was observed that an adenosine derivative, IFC-305 favor the hepatic tissue remodeling , modulates the energetic state (Pérez-Carreón JI, 2010; Master thesis Pérez-Cabeza de Vaca, 2010) and immune response in hepatoxicity, this suggest a possible role of the IFC-305 against the injuries that take place during MI. EXPERIMENTAL MODEL: Male rats Wist ar of 200g receive a subcutaneous administration of ISO 67mg/kg, and one hour after they receive an IFC-305 intraperitoneal injection. We worked wi th the following groups: 1. Control (Saline solution), 2. ISO, 3.IFC and 4. ISO+IFC. Rats sacrifice was performed 6, 12, 24 or 96 hours after ISO administration. Hearts and plasma samples were recollected. We evaluated the levels of IL 1β, IL-6, INFγ, T NFα, and IL 10, in male Wist ar rat plasma and heart, through every stage of the infarction process induced by isoproterenol. The results s how alterations in the former cytokines levels as consequence of isoproterenol administration. Also, the restoration of the physiological levels of these cytokines was reached with the administration of an adenosine derivative: IFC-305. In conclusion, our results show evident alterations in cytokines levels as reflect of immune response that take place during the MI and that the IFC-305 is able to modulate this response in a favorable way. Still, there are necessary more studies about the immnunomodulatory role of the IFC-305 during MI.
