Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine

• Autores: Míriam Navarro Sobrino, Jordi Lorita, María Soley i Farrés, I. Ramírez
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 25, Nº. 5, 2010, págs. 589-597
• Idioma: inglés
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• Resumen

  • The involvement of catecholamines in stress-induced heart injury is well documented. However, the contribution of adrenergic receptor types is less understood. Both the profile of plasma marker enzyme activities (lactate dehydrogenase-1 ans aspartate transaminase) and the distribution and morphology of the lesions observed in tissue sections of adrenaline-injucted mice resembled those of stressed (restraint and cold exposed) mice. Next, we compared the effect of isoproterenol (ß-adrenergic agonist) and phenylephrine (a1-adrenergic agonist) on both heart function and tissue injury. In Langendorff-perfused rat hearts, a1-adrenergic receptors made a minor contribution to the tonic effect of adrenaline, as indicated by the lack of effect on the heart rate and the delayed negative inotropic effect of phenylephrine. However, in whole mice, phenylephrine but not isoproterenol, induced an increase of both lactate dehydrogenase-1 and aspartate transaminase activities. Hearts of phenylephrine-injected mice showed necrotic lesions in subendocardial areas of the left ventricle. In addition a scattered focal leukocyte infiltration around single apoptotic-like myocytes was observed in the ventricle wall. Hearts of isoproterenol-injected mice showed a similar numbre of apoptotic-like myocytes, but a much lower numbre of necrotic areas, than phenylephrine-injected animals. Our results suggest that the cardiotonic effect of catecholamines involves mainly the ß-adrenergic receptors. However, the acute catecholamine-induced heart injury involves mainly a1-adrenergic receptors.