Document Detail

Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics.
MedLine Citation:
PMID:  19734357     Owner:  NLM     Status:  MEDLINE    
We investigated left ventricular (LV) mechanical work and energetics in the cross-circulated (blood-perfused) isoproterenol [Iso 1.2 mg x kg(-1).day(-1) for 3 days (Iso3) or 7 days (Iso7)]-induced hypertrophied rat heart preparation under isovolumic contraction-relaxation. We evaluated pressure-time curves per beat, end-systolic pressure-volume and end-diastolic pressure-volume relations, and myocardial O(2) consumption per beat (Vo(2))-systolic pressure-volume area (PVA; a total mechanical energy per beat) linear relations at 240 beats/min, because Iso-induced hypertrophied hearts failed to completely relax at 300 beats/min. The LV relaxation rate at 240 beats/min in Iso-induced hypertrophied hearts was significantly slower than that in control hearts [saline 24 microl/day for 3 and 7 days (Sa)] with unchanged contraction rate. The Vo(2)-intercepts (composed of basal metabolism and Ca(2+) cycling energy consumption in excitation-contraction coupling) of Vo(2)-PVA linear relations were unchanged associated with their unchanged slopes in Sa, Iso3, and Iso7 groups. The oxygen costs of LV contractility were also unchanged in all three groups. The amounts of expression of sarcoplasmic reticulum Ca(2+)-ATPase, phospholamban (PLB), phosphorylated-Ser(16) PLB, phospholemman, and Na(+)-K(+)-ATPase are significantly decreased in Iso3 and Iso7 groups, although the amount of expression of NCX1 is unchanged in all three groups. Furthermore, the marked collagen production (types I and III) was observed in Iso3 and Iso7 groups. These results suggested the possibility that lowering the heart rate was beneficial to improve mechanical work and energetics in isoproterenol-induced hypertrophied rat hearts, although LV relaxation rate was slower than in normal hearts.
Chikako Nakajima-Takenaka; Guo-Xing Zhang; Koji Obata; Kiyoe Tohne; Hiroko Matsuyoshi; Yukiko Nagai; Akira Nishiyama; Miyako Takaki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-09-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  297     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-27     Completed Date:  2009-11-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1736-43     Citation Subset:  IM    
Department of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, Japan.
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MeSH Terms
Adrenergic beta-Agonists / administration & dosage
Blood Pressure
Blotting, Western
Calcium-Binding Proteins / metabolism
Cardiomegaly / chemically induced,  metabolism*,  physiopathology*
Collagen Type I / genetics,  metabolism
Collagen Type III / genetics,  metabolism
Coronary Circulation
Disease Models, Animal
Energy Metabolism*
Heart Rate
Infusion Pumps, Implantable
Isoproterenol / administration & dosage
Membrane Proteins / metabolism
Myocardial Contraction*
Myocardium / metabolism*
Oxygen Consumption*
Phosphoproteins / metabolism
Polymerase Chain Reaction
RNA, Messenger / metabolism
Rats, Wistar
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
Sodium-Calcium Exchanger / metabolism
Sodium-Potassium-Exchanging ATPase / metabolism
Time Factors
Ventricular Function, Left*
Ventricular Pressure
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Calcium-Binding Proteins; 0/Collagen Type I; 0/Collagen Type III; 0/Membrane Proteins; 0/Phosphoproteins; 0/RNA, Messenger; 0/Sodium-Calcium Exchanger; 0/phospholamban; 0/sodium-calcium exchanger 1; 135541-82-1/phospholemman; 56-45-1/Serine; 7683-59-2/Isoproterenol; EC Reticulum Calcium-Transporting ATPases; EC ATPase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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