|Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics.|
|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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|Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-09-04|
|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|
|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|
|Languages: eng Pagination: H1736-43 Citation Subset: IM|
|Department of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, Japan.|
|APA/MLA Format Download EndNote Download BibTex|
administration & dosage
Calcium-Binding Proteins / metabolism
Cardiomegaly / chemically induced, metabolism*, physiopathology*
Collagen Type I / genetics, metabolism
Collagen Type III / genetics, metabolism
Disease Models, Animal
Infusion Pumps, Implantable
Isoproterenol / administration & dosage
Membrane Proteins / metabolism
Myocardium / metabolism*
Phosphoproteins / metabolism
Polymerase Chain Reaction
RNA, Messenger / metabolism
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
Sodium-Calcium Exchanger / metabolism
Sodium-Potassium-Exchanging ATPase / metabolism
Ventricular Function, Left*
|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 22.214.171.124/Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 126.96.36.199/Sodium-Potassium-Exchanging ATPase|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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