title: [The activation of A1 adenosine receptors attenuates myocardial stunning in the rabbit].
abstract: Hearts exposed to a prolonged period of ischemia (> or = 30 minutes) present smaller infarct size when reperfused in the presence of adenosine. However, when the period of ischemia is shorter, the infarct areas are not very significant, but a postischemic ventricular dysfunction persists. The objective of this study was to determine the effect of adenosine, (administered only during reperfusion) on systolic and diastolic alterations present in postischemic ventricular dysfunction, as well as to determine whether A1 receptors participate in this effect. Isolated isovolumic rabbit hearts were subjected to 15 minutes of global ischemia followed by 30 minutes of reperfusion. Before ischemia and during reperfusion ventricular function was evaluated. In the control group, the left ventricular developed pressure (LVDP) reached 56 +/- 2% of recovery at 30 minutes of reperfusion. The administration of adenosine improved LVDP 75 +/- 3% (P < 0.05 vs. control). However, when adenosine was given in presence of an A1 receptor selective antagonist (DPCPX), LVDP reached 50 +/- 2% (P < 0.05 vs. control). In the control group, left ventricular end diastolic pressure (LVEDP) (diastolic stiffness), increased 293 +/- 4%, at 30 minutes of reperfusion. Only a 15 +/- 8% (P < 0.05 vs. control) increase in LVEDP was observed with adenosine. Reperfusion with adenosine plus DPCPX did not attenuate an increase of 493 +/- 9% (P < 0.05 vs. control) in diastolic stiffness. Adenosine administered from the beginning of reperfusion attenuated both systolic alterations and diastolic stiffness in postischemic dysfunction. This effect was abolished by DPCPX, suggesting an important role for the A1 receptors in adenosine protection.
authors.affiliation: Laboratorio de Fisiopatología Cardiovascular, Departamento de Patología, Facultad de Medicina, Universidad de Buenos Aires y Fundación Grupo de Estudios Multicéntricos en Argentina (GEMA), Buenos Aires, Argentina.
authors.forename: M
authors.initials: M
authors.lastname: Donato
authors.forename: C
authors.initials: C
authors.lastname: Morales
authors.forename: V
authors.initials: V
authors.lastname: D'Annunzio
authors.forename: O
authors.initials: O
authors.lastname: Scapín
authors.forename: R J
authors.initials: RJ
authors.lastname: Gelpi
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D009200:Myocardial Contraction / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000150:complications; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000150:complications; D017682:Myocardial Stunning / Q000503:physiopathology / Q000517:prevention & control*; D058915:Purinergic P1 Receptor Antagonists; D011817:Rabbits; D018047:Receptors, Purinergic P1 / Q000502:physiology*; D013997:Time Factors; D014665:Vasodilator Agents / Q000494:pharmacology*; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D058915:Purinergic P1 Receptor Antagonists; D018047:Receptors, Purinergic P1; D014665:Vasodilator Agents; D000241:Adenosine