Acute initial haemodynamic changes in a rat isoprenaline model of cardiotoxicity
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
22381740
DOI
10.1177/0960327112438927
PII: 0960327112438927
Knihovny.cz E-zdroje
- MeSH
- agonisté adrenergních beta-receptorů toxicita MeSH
- funkce levé komory srdeční účinky léků MeSH
- hemodynamika účinky léků MeSH
- isoprenalin toxicita MeSH
- kardiotoxiny toxicita MeSH
- krysa rodu Rattus MeSH
- modely nemocí na zvířatech MeSH
- potkani Wistar MeSH
- srdce účinky léků fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- agonisté adrenergních beta-receptorů MeSH
- isoprenalin MeSH
- kardiotoxiny MeSH
The synthetic catecholamine isoprenaline (ISO) has been used as an inductor in the acute myocardial infarction model for more than a half century. Despite the fact that many articles were published on this topic, precise early haemodynamic pathology remains unknown. Acute haemodynamic changes were measured in rats; first, in preliminary experiments by the thermodilution method; and second, in main experiments continuously for 2 h using a Millar catheter. Animals received saline or ISO in the cardiotoxic dose (100 mg/kg, subcutaneously). Also, additional experiments were performed with salbutamol in order to evaluate the role of β(2)-receptors. ISO caused a rapid, within 1 min, approximately 40% decrease in arterial blood pressures, 30% increase in the heart rate, and 30% decrease in the stroke volume. Within the first 2 min, the changes were followed by decreases in afterload (-40%), preload (-10%), diastolic relaxation (-50%), diastolic filling (-40%), and a marked, but short-term, increase in the left ventricle contractility (+100%). Ejection fraction did not significantly change, suggesting diastolic dysfunction. Salbutamol, with the exception of diastolic pressure and afterload, did not substantially influence other parameters. In conclusion, this study demonstrated that diastolic dysfunction precedes systolic dysfunction and β(2)-receptor stimulation alone is not sufficient for an early induction of diastolic dysfunction.
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