Enhancement of contractility with sustained afterload in the intact murine heart: blunting of length-dependent activation.
Enhancement of contractility with sustained afterload in the intact murine heart: blunting of length-dependent activation.
复制标题
完整小鼠心脏持续后负荷增强收缩力：减弱长度依赖性激活。
DOI：
10.1161/01.cir.0000070964.96190.67
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发表时间：
2003
期刊：
影响因子：
37.8
通讯作者：
Feldman,MarcD
中科院分区：
文献类型：
--
作者：
Reyes,Maricela;Freeman,GregoryL;Escobedo,Daniel;Lee,Shuko;Steinhelper,MarkE;Feldman,MarcD
背景--有人假设，由于其心率很快，完整的小鼠心脏在基础状态下的收缩能力接近最大。如果这一假设是正确的，那么与较大的哺乳动物相比，心肌长度依赖的激活的快慢成分应该被钝化。方法和结果-麻醉小鼠(n=24)，通过开胸通过双频电导导管系统确定左心室压力-容量关系。在短暂阻断下腔静脉时测定基线压力-容量关系，并在持续阻断主动脉1分钟(n=10)和7分钟(n=21)后重复测量。对照实验在一组小鼠身上进行(n=3)。在基线至1min时，增加后负荷(最大压力95±9至126±7 mm Hg；P<；0.001)和有效动脉弹性(5.9±3.1至9.2±3.9 mm Hg/μL；P<；0.001)导致舒张末容量增加(31±8至35±9μL；P<；0.001)。结果是由于收缩能力的增加(收缩末期弹性V100左移，24±9至16±5μL；P<；0.001)，每搏量得以维持(17±6至15±6；P=NS)。7分钟后未发现收缩功能的进一步增强。结论--本研究表明，长度依赖激活的快相是完整的，但慢相不是完整的，与基础状态下接近最大收缩能力的小鼠心肌功能一致。
Background—It has been hypothesized that because of its rapid heart rate, the intact murine heart functions near maximal contractility in the basal state. If this hypothesis is correct, then the fast and slow components of myocardial length-dependent activation should be blunted compared with larger mammals.Methods and Results—Mice (n=24) were anesthetized, and via an open chest, LV pressure-volume relationships were determined by a dual-frequency conductance catheter system. Baseline pressure-volume relationships were determined during transient occlusion of the inferior vena cava, and repeat measurements were made after 1 (n=10) and 7 (n=21) minutes of sustained aortic occlusion. Control experiments were performed in a subset of mice (n=3). For baseline to 1 minute, an increase in afterload (maximal pressure 95±9 to 126±7 mm Hg;P<0.001) and effective arterial elastance (5.9±3.1 to 9.2±3.9 mm Hg/μl;P<0.001) resulted in an increase in end-diastolic volume (31±8 to 35±9 μL;P<0.001). The result was maintenance of stroke volume (17±6 to 15±6;P=NS) owing to an increase in contractility (leftward shift in V100[the volume of end-systolic elastance at 100 mm Hg], 24±9 to 16±5 μL;P<0.001). No additional augmentation of systolic function was found at 7 minutes.Conclusions—This study demonstrates that the fast phase of length-dependent activation is intact but not the slow phase, consistent with murine myocardium functioning near maximal contractility in the basal state.