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Cardiac biomarkers in a model of acute catecholamine cardiotoxicity

Pemysl Mladnka

Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic, mladenkap{at}faf.cuni.cz

Radomír Hrdina

Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Zuzana Bobrovová

Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Vladimír Semeck

Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Jaroslava Vávrová

Institute of Clinical Biochemistry and Diagnostics, Faculty of Medicine in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Magdaléna Holeková

Institute of Clinical Biochemistry and Diagnostics, Faculty of Medicine in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Vladimir Palicka

Institute of Clinical Biochemistry and Diagnostics, Faculty of Medicine in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Yvona Mazurová

Department of Histology and Embryology, Faculty of Medicine in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Petr Nachtigal

Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic

Coronary heart disease and in particular its most serious form — acute myocardial infarction (AMI) — represents the most common cause of mortality in developed countries. Better prognosis may be achieved by understanding the etiopathogenetic mechanisms of AMI. Therefore, a catecholamine model of myocardial injury, which has appeared to be very similar to AMI in human in some aspect, was used. Male Wistar:Han rats were randomly divided into two groups: control group (saline) and isoprenaline group (ISO; synthetic catecholamine, 100 mg.kg^{— 1} subcutaneously [s.c.]). After 24 hours, functional parameters were measured, biochemical markers in the blood and metals content in the heart tissue were analysed and histological examination was performed. ISO caused marked myocardial injury that was associated with myocardial calcium overload. Close correlation between myocardial impairment (i.e. serum TnT, stroke volume index and wet ventricles weight) and the levels of myocardial calcium was observed. Direct reactive oxygen species (ROS) involvement was documented only by non-significant increase in malonyldialdehyde 24 hours after ISO injury. Moreover, myocardial element analysis revealed no significant changes as for the content of zinc and iron while selenium and copper increased in the ISO group although it reached statistical significance only for the latter.

Key Words: Isoprenaline • acute myocardial infarction • calcium overload • cardiac troponin T • reactive-oxygen species • microelement

This version was published on October 1, 2009

Human & Experimental Toxicology, Vol. 28, No. 10, 631-640 (2009)
DOI: 10.1177/0960327109350665


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