கார்டியோவாஸ்குலர் மருந்தியல்: திறந்த அணுகல்

சுருக்கம்

Isoproterenol-Induced Intramural Cytotoxicity Does Not Correlate with Echocardiographic Functional Abnormalities in Wistar Rat Hearts

Luciane Filla, Julio Cesar Francisco, Rossana Baggio Simeoni, Nelson Itiro Myiague, Ana Carolina. Irioda, Reginaldo Justino Ferreira, Marcia Olandoski, Luiz Cesar Guarita-Souza, Eltyeb Abdelwahid and Katherine Athayde Teixeira de Carvalho

Background: Isoproterenol (ISO) is a potent non-selective beta-adrenergic agonist with very low affinity for alpha-adrenergic receptors used for treatment of various cardiac problems including ventricular arrhythmias, asthma and shock. In addition, ISO is also used postoperatively after cardiac surgery. The aim of this study was to analyze the association between histopathological and functional effects of ISO in the rat myocardium. Methods: 24 Wistar rats (healthy, males) were used in these experiments. The animals were randomly divided two groups. Group I (n=12): all animals received ISO subcutaneous administration (0,3 mg/Kg/day for 8 days). Group II (n=12): all animals received Phosphate Buffered Saline (PBS) subcutaneous administration as a control. One day after drug administration has been completed; echocardiographic analysis of cardiac function was performed. Histopathological analysis of the specimens was made by using H&E, Gomori’s Trichrome and picrosirius red staining procedures. The results were analyzed using Student’s t-test (p<0,05). Results: Our histopathological results demonstrated: presence of diffuse inflammation, necrosis and fibrosis in the myocardium, and hypertrophy of ventricular septum. Interestingly, we did not find significant alteration in cardiac function (p>0.05), however the heart rate differed significantly between both groups (p=0.0053). Conclusion: Short-term ISO administration (8 days) caused notable intramural cytotoxicity of the heart. In contrast, echocardiographic findings did not show any functional abnormalities in accordance with this cytotoxicity.