INCREASED MYOTHERMAL ECONOMY OF ISOMETRIC FORCE GENERATION IN COMPENSATED CARDIAC-HYPERTROPHY INDUCED BY PULMONARY-ARTERY CONSTRICTION IN THE RABBIT - A CHARACTERIZATION OF HEAT LIBERATION IN NORMAL AND HYPERTROPHIED RIGHT VENTRICULAR PAPILLARY-MUSCLES
INCREASED MYOTHERMAL ECONOMY OF ISOMETRIC FORCE GENERATION IN COMPENSATED CARDIAC-HYPERTROPHY INDUCED BY PULMONARY-ARTERY CONSTRICTION IN THE RABBIT - A CHARACTERIZATION OF HEAT LIBERATION IN NORMAL AND HYPERTROPHIED RIGHT VENTRICULAR PAPILLARY-MUSCLES
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DOI：
10.1161/01.res.50.4.491
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发表时间：
1982-01-01
影响因子：
20.1
通讯作者：
MULIERI, LA
中科院分区：
文献类型：
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作者：
ALPERT, NR;MULIERI, LA
在正常和肥大的乳头肌中测量初始、恢复和静息热，以监测伴随肥大的亚细胞变化的能量后果。测量前4周，兔肺动脉收缩。以0.2 Hz、21度刺激右心室乳头肌。C在等长条件下的克雷布斯-林格溶液中的最佳长度。峰值抽搐张力为5.90 +-。0.25 g/mm2 （SEM[平均值的标准误差]）在正常肌肉(N)和5.11。0.47 g/mm2 （NS[无统计学意义]）。最大张力产生率比15.9 +-降低了26% （P < 0.02）。0.85 g/mm2 s (N) ~ 11.7。1.37 g/mm2 s (P)。峰值张力时间从627 +-增加30% （P < 0.001）。20 m (N) ~ 816 .+-。21米(P)。每跳动总活动相关发热量从3.92±-下降了36% （P < 0.001）。0.26 mcal/g (N) ~ 2.51。0.29 mcal/g (P)初始热从1.66±-降低了37% （P < 0.001）。0.10 mcal/g (N) ~ 1.04。0.12 mcal/g (P)。等长热系数比8.76 +-提高了43% （P < 0.005）。0.54 (N) ~ 12.5。1 (P)显示肥厚的经济性增加。早期为快速阶段（1.29 .+-）。0.12 McAl /g /)的初热，持续时间为396 +-。25米，这与张力积累有关。缓慢阶段(1.05 .+-。0.07 McAl /g / s)。肥厚组快速期较正常慢32% (P < 0.05)，持续时间延长27% (P < 0.02)；慢期较正常慢48% （P < 0.001）。回收量与初热的比值(1.37 .+-。0.09)， N、P肌组差异无统计学意义。静息热为2.08±-。0.35 mcal/g / N和1.35 .+-。P肌每拍0.23 mcal/g。目前的结果和以往的酶学和力学研究表明，代偿性压力过载肥厚与正常心脏之间的关系类似于慢速骨骼肌与快速骨骼肌之间的关系。由压力过载引起的心脏肥厚变化是有益的，因为它们满足了新的血流动力学要求，增加了力产生的经济性。
Initial, recovery and resting heat were measured in normal and hypertrophied papillary muscles in order to monitor the energetic consequences of the subcellular changes accompanying hypertrophy. The pulmonary artery was constricted in rabbits 4 wk prior to measurements. Right ventricular papillary muscles were stimulated at 0.2 Hz and 21.degree. C in Krebs-Ringer solution under isometric conditions at optimum length. Peak twitch tension was 5.90 .+-. 0.25 g/mm2 (SEM [standard error of the mean]) in normal muscle (N) and 5.11 .+-. 0.47 g/mm2 (NS [not significant]) in pressure overload muscle (P). The maximal rate of tension generation decreased 26% (P < 0.02) from 15.9 .+-. 0.85 g/mm2 s (N) to 11.7 .+-. 1.37 g/mm2 s (P). Time-to-peak tension increased 30% (P < 0.001) from 627 .+-. 20 m (N) to 816 .+-. 21 m (P). The total activity related heat production per beat decreased 36% (P < 0.001) from 3.92 .+-. 0.26 mcal/g (N) to 2.51 .+-. 0.29 mcal/g (P). Initial heat was reduced 37% (P < 0.001) from 1.66 .+-. 0.10 mcal/g (N) to 1.04 .+-. 0.12 mcal/g (P). The isometric heat coefficient increased 43% (P < 0.005) from 8.76 .+-. 0.54 (N) to 12.5 .+-. 1 (P) showing increased economy in hypertrophy. There was an early fast phase (1.29 .+-. 0.12 mcal/g per) of initial heat lasting 396 .+-. 25 m which was related to tension build-up. A slow phase (1.05 .+-. 0.07 mcal/g per s) accompanied relaxation. In hypertrophy, the fast phase was 32% (P < 0.05) slower than normal and lasted 27% (P < 0.02) longer; the slow phase was 48% (P < 0.001) slower than normal. The ratio of recovery to initial heat (1.37 .+-. 0.09) was not different in N and P muscles. Resting heat was 2.08 .+-. 0.35 mcal/g per beat in N and 1.35 .+-. 0.23 mcal/g per beat in P muscles. Present results and previous enzymatic and mechanical studies suggest that the relation between the compensated pressure overload hypertrophied and normal hearts is similar to the relation between slow and fast skeletal muscle. The changes in the heart that undergoes hypertrophy secondary to pressure overload are beneficial, since they meet the new hemodynamic demands with increased economy of force production.