Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice
Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice
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DOI：
10.1152/ajpheart.2001.281.5.h1938
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发表时间：
2001-11-01
影响因子：
4.8
通讯作者：
Redfield, MM
中科院分区：
文献类型：
--
作者：
Hart, CYT;Burnett, JC;Redfield, MM
在评估小鼠心脏结构和功能的研究中，常用的麻醉方案是赛拉津-氯胺酮(XK)和阿维汀(AV)。虽然已经知道XK麻醉会在小鼠身上产生更多的心动过缓，但XK和AV对心功能的影响还没有进行比较。我们用XK或AV麻醉正常成年雄性瑞士Webster小鼠。应用经胸超声心动图和闭合胸心导管法测定心率(HR)、舒张末和收缩末期左室内径(LVDd和LVds)、短轴缩短率(FS)、左心室舒张末压(LVEDP)、等容舒张期时间常数(Tau)和左室压升降一阶导数(dp/dt(Max)和dp/dt(Min))。在超声心动图中，XK组小鼠的心率低于AV组(250+/-14次/分钟比453+/-24次/分钟，P<0.05)。XK组小鼠的前负荷增加(XK组为4.1+/-0.08 mm，房室组为3.8+/-0.09 mm，P<0.05)。XK小鼠收缩功能的负荷依赖性指标FS增加(XK组为45+/-1.2%，AV组为40+/-0.8%，P<；0.05)。在LV插管时，两种麻醉的心率差异较大，房室(453+/-24次/min)和XK(342+/-30次/min，P<；0.05)，收缩或舒张期功能在两组间差异无统计学意义。然而，在心率为300次/分的XK小鼠中，收缩功能(LV dp/dt(Max)：4,402+/-798比8,250+/-415 mm Hg/S)和舒张期功能(：23+/-2ms比14+/-1ms，P<；0.05)受到损害。与房室心动过缓相比，心动过缓对负荷状态和心功能均有影响。超声心动图和左心导管术的不同发现强调了全面评估小鼠左心功能的重要性。
Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (tau), and the first derivatives of LV pressure rise and fall (dP/dt(max) and dP/dt(min), respectively). During echocardiography, HR was lower in XK than AV mice (250 +/- 14 beats/min in XK vs. 453 +/- 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 +/- 0.08 mm in XK vs. 3.8 +/- 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 +/- 1.2% in XK vs. 40 +/- 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 +/- 24 beats/min) and XK (342 +/- 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR 300 beats/min, P < 0.05), whereas systolic (LV dP/dt(max): 4,402 +/- 798 vs. 8,250 +/- 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (: 23 +/- 2 vs. 14 +/- 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.