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Differential right and left ventricular diastolic tolerance to acute afterload and NCX gene expression in Wistar rats
J. Correia-Pinto, T. Henriques-Coelho, R. Roncon-Albuquerque Jr, A. F. Leite-Moreira
Jazyk angličtina Země Česko
Typ dokumentu srovnávací studie
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- diastola fyziologie genetika MeSH
- exprese genu genetika MeSH
- financování vládou MeSH
- hemodynamika fyziologie genetika MeSH
- interpretace statistických dat MeSH
- polymerázová řetězová reakce s reverzní transkripcí metody využití MeSH
- potkani Wistar fyziologie genetika MeSH
- pumpa pro výměnu sodíku a vápníku genetika MeSH
- srdce - funkce komor fyziologie genetika MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- srovnávací studie MeSH
This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant ??and end diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV-?, but increased RV-?. Whereas LV-? analyzed the major course of pressure fall, RV-? only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50 % lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca2+ reuptake, late relaxation and diastolic dysfunction.
Grant č. 47519 POCTI/CBO -- Grant č. 61547 POCI/SAU-MMO -- Grant č. 51 FCT
Bibliografie atd.Lit.: 49
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- $a This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant ??and end diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV-?, but increased RV-?. Whereas LV-? analyzed the major course of pressure fall, RV-? only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50 % lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca2+ reuptake, late relaxation and diastolic dysfunction.
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