抄録
We investigated left ventricular (LV) mechanical work and energetics in the cross-circulated (blood-perfused) isoproterenol (Iso 1.2 mg/kg/day for 3 or 7 days)-induced hypertrophied rat heart preparation under isovolumic contraction-relaxation. [Methods] We evaluated pressure-time curves per beat, end-systolic pressure-volume and end-diastolic pressure-volume relations, and myocardial O2 consumption per beat (VO2)-systolic pressure-volume area (PVA; a total mechanical energy per beat) linear relations. [Results] The LV relaxation rate at 240 bpm in Iso-induced hypertrophied hearts was significantly slower than that in control hearts (saline 24 μl/day for 3 or 7 days) with unchanged contraction rate. Interestingly, the relaxation half-time (T1/2) was not prolonged by increasing LV volume in Iso-induced hypertrophied hearts, although it was prolonged in control hearts. Although the expression of Ca2+ cycling proteins, the ratio of sarcoplasmic reticulum Ca2+-ATPase versus phospholamban (SERCA2A/PLB) expression and Na+-Ca2+ exchanger (NCX1) expression, and the VO2-intercept (summation of basal metabolism and Ca2+ cycling energy consumption) of VO2-PVA linear relation was unchanged, the collagen production (type I and III) was markedly enhanced in Iso-induced hypertrophied hearts. [Conclusion] The present results suggested the possibility that LV lusitropic dysfunction of isoproterenol-induced hypertrophied rat heart is due to marked collagen production but not due to Ca2+ cycling impairment. [J Physiol Sci. 2007;57 Suppl:S209]
