-
Something wrong with this record ?
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
Language English Country Czech Republic
Document type Comparative Study
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Diastole physiology genetics MeSH
- Gene Expression genetics MeSH
- Financing, Government MeSH
- Hemodynamics physiology genetics MeSH
- Data Interpretation, Statistical MeSH
- Reverse Transcriptase Polymerase Chain Reaction methods utilization MeSH
- Rats, Wistar physiology genetics MeSH
- Sodium-Calcium Exchanger genetics MeSH
- Ventricular Function physiology genetics MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Comparative Study 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.
References provided by Crossref.org
Grant č. 47519 POCTI/CBO -- Grant č. 61547 POCI/SAU-MMO -- Grant č. 51 FCT
Bibliography, etc.Lit.: 49
- 000
- 03364naa 2200457 a 4500
- 001
- bmc07500525
- 003
- CZ-PrNML
- 005
- 20111210120856.0
- 008
- 070724s2006 xr e eng||
- 009
- AR
- 024 __
- $a 10.33549/physiolres.930845 $2 doi
- 035 __
- $a (PubMed)16343035
- 040 __
- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Correia-Pinto, J.
- 245 10
- $a Differential right and left ventricular diastolic tolerance to acute afterload and NCX gene expression in Wistar rats / $c J. Correia-Pinto, T. Henriques-Coelho, R. Roncon-Albuquerque Jr, A. F. Leite-Moreira
- 314 __
- $a Department of Physiology, Faculty of Medicine, University of Porto, Porto
- 500 __
- $a Grant č. 47519 POCTI/CBO -- Grant č. 61547 POCI/SAU-MMO -- Grant č. 51 FCT
- 504 __
- $a Lit.: 49
- 520 9_
- $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.
- 650 _2
- $a pumpa pro výměnu sodíku a vápníku $x genetika $7 D019831
- 650 _2
- $a exprese genu $x genetika $7 D015870
- 650 _2
- $a srdce - funkce komor $x fyziologie $x genetika $7 D016276
- 650 _2
- $a diastola $x fyziologie $x genetika $7 D003971
- 650 _2
- $a hemodynamika $x fyziologie $x genetika $7 D006439
- 650 _2
- $a potkani Wistar $x fyziologie $x genetika $7 D017208
- 650 _2
- $a polymerázová řetězová reakce s reverzní transkripcí $x metody $x využití $7 D020133
- 650 _2
- $a interpretace statistických dat $7 D003627
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a financování vládou $7 D005380
- 655 _2
- $a srovnávací studie $7 D003160
- 700 1_
- $a Henriques-Coelho, T.
- 700 1_
- $a Roncon-Albuquerque, R. $c Jr.
- 700 1_
- $a Leite-Moreira, A. F.
- 773 0_
- $w MED00003824 $t Physiological research $g Roč. 55, č. 5 (2006), s. 513-526 $x 0862-8408
- 856 41
- $u https://www.biomed.cas.cz/physiolres/pdf/55/55_513.pdf $y plný text volně přístupný
- 910 __
- $y 1 $a ABA008 $b A 4120 $c 266
- 990 __
- $a 20070723155916 $b ABA008
- 991 __
- $a 20070904130836 $b ABA008
- 999 __
- $a ok $b bmc $g 616139 $s 468571
- BAS __
- $a 3
- BMC __
- $a 2006 $b 55 $c 5 $d 513-526 $i 0862-8408 $m Physiological research $x MED00003824
- LZP __
- $a 2007-5/mkal
