Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics.
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.
Nakajima-Takenaka
Chikako
C
Department of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, Japan.
Zhang
Guo-Xing
GX
Obata
Koji
K
Tohne
Kiyoe
K
Matsuyoshi
Hiroko
H
Nagai
Yukiko
Y
Nishiyama
Akira
A
Takaki
Miyako
M
D000318:Adrenergic beta-Agonists / Q000008:administration & dosage; D000818:Animals; D001794:Blood Pressure; D015153:Blotting, Western; D002135:Calcium-Binding Proteins / Q000378:metabolism; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D024061:Collagen Type III / Q000235:genetics / Q000378:metabolism; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004734:Energy Metabolism; D006339:Heart Rate; D015918:Infusion Pumps, Implantable; D007545:Isoproterenol / Q000008:administration & dosage; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion; D010750:Phosphoproteins / Q000378:metabolism; D010766:Phosphorylation; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D012694:Serine; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D000099211:Phospholamban
D000318:Adrenergic beta-Agonists; D002135:Calcium-Binding Proteins; D024042:Collagen Type I; D024061:Collagen Type III; D007545:Isoproterenol; D008565:Membrane Proteins; D010750:Phosphoproteins; D012333:RNA, Messenger; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D012694:Serine; D019831:Sodium-Calcium Exchanger; D000254:Sodium-Potassium-Exchanging ATPase; D000099211:Phospholamban; C110374:sodium-calcium exchanger 1; C069141:phospholemman