Ultrastructural and functional aspects of frog heart lesions after isoproterenol.

The purpose of the present study was to explore the possible correlation between the ultrastructural changes and the functional changes induced by isoproterenol (IPR) in the myocardium of the frog. The study was performed on winter frogs (R. pipiens), The experimental animals wend then given 2 daily doses of IPR (200 mg/kg b,w.). Twenty-four hours after the second IPR dose, specimens were taken from the heart ventricle and subjected to electron microscopical examination and to analysis of the isometric force decay in response to anoxia produced by sodium cyanide. Specimens were taken from macroscopically non-damaged portions of the ventricle as well as from aneurysms. Control animals were kept at + 8 degrees C and + 25 degrees C and injected with saline. In all IPR-injected animals the specimens from macroscopically non-damaged parts of the myocardium showed ultrastructural changes characterized by a relative increase in mitochondrial mass and a pronounced reduction of glycogen. Specimens from aneurysms showed similar changes but in some fibres signs of more severe injury were observed such as fragmentation of the cristae of the mitochondria and disintegration of myofibrils. The functional analyses showed that the isometric force decay of the heart muscle strips induced by the respiratory block by cyanide was much greater in specimens from IPR-treated animals than in those from control frogs. The augmented force decay was found in both strips from macroscopically normal parts of the myocardium and in those from aneurysms although it was somewhat greater and more rapid in the latter. The observed, minor functional difference between macroscopically non-damaged portions of the myocardium and aneurysms is remarkable with respect to the different preservation of myofilaments in these regions. This similarity in functional decline could possibly be due to the observed homogenous reduction of glycogen in the IPR-exposed myocardium since glycogen was the only source of ATP under the experimental conditions of current interest.