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Cardiac biomarkers in a model of acute catecholamine cardiotoxicity
P. Mladenka, R. Hrdina, Z. Bobrovova, V. Semecky, J. Vavrova, M. Holeckova, V. Palicka, Y. Mazurova, P. Nachtigal
Language English Country Great Britain
Document type Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 1998-01-01 to 2015-12-31
SAGE Publications Journals
from 1999-01-01 to 2015-12-31
Nursing & Allied Health Database (ProQuest)
from 1998-01-01 to 2015-12-31
Health & Medicine (ProQuest)
from 1998-01-01 to 2015-12-31
- MeSH
- Antioxidants metabolism MeSH
- Biomarkers analysis blood metabolism MeSH
- Heart Function Tests MeSH
- Myocardial Infarction diagnosis chemically induced blood metabolism MeSH
- Catecholamines toxicity MeSH
- Blood Pressure drug effects MeSH
- Rats MeSH
- Ascorbic Acid blood MeSH
- Disease Models, Animal MeSH
- Myocardium metabolism pathology MeSH
- Rats, Wistar MeSH
- Reactive Oxygen Species metabolism MeSH
- Heart Rate drug effects MeSH
- Heart Ventricles metabolism pathology drug effects MeSH
- Troponin T blood MeSH
- Calcium metabolism MeSH
- Organ Size drug effects MeSH
- Vitamin E blood MeSH
- Iron metabolism toxicity MeSH
- Zinc metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
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.
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- $a 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.
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