Palakodeti V, Oh S, Oh B H, Mao L, Hongo M, Peterson K L, Ross J
Department of Medicine, University of California San Diego, La Jolla 92093-0613, USA.
Am J Physiol. 1997 Sep;273(3 Pt 2):H1283-90. doi: 10.1152/ajpheart.1997.273.3.H1283.
The effects of heart rate (HR) on myocardial contractility in the mouse heart in situ were first investigated in open-chest mice (n = 7) by left ventricular (LV) catheter-tip micromanometry. HR was first slowed with a sinus node inhibitor (zatebradine), and atrial pacing to progressively increase the HR caused a positive inotropic response (assessed by maximum positive first derivative of LV pressure, LV dP/dtmax) up to a HR of 282 beats/min with the onset of a descending limb of the force-frequency relation (FFR) at 332 beats/min. beta-Adrenergic receptor stimulation (dobutamine) shifted upward and significantly steepened the positive FFR and increased HR at the onset of the descending limb to 402 beats/min. HR and LV dP/dtmax were then studied in closed-chest mice without pacing during recovery from anesthesia (n = 7), and during rest and intermittent physical activity the FFR was linear and positive up to 600 beats/min. HR was then progressively slowed with zatebradine, and the points at rest and during activity fell on the same linear relation. Thus we conclude the following: 1) in the open-chest anesthetized mouse, a positive FFR was amplified by beta-adrenergic receptor stimulation, and 20 in the mouse recovering from anesthesia the sinus node rate remained a critical determinant of myocardial contractility, without a descending limb of the FFR.
通过左心室（LV）导管尖端微测法，首先在开胸小鼠（n = 7）中研究了心率（HR）对原位小鼠心脏心肌收缩力的影响。首先用窦房结抑制剂（扎替雷定）减慢心率，然后通过心房起搏逐渐增加心率，导致正性肌力反应（通过左心室压力的最大正一阶导数，LV dP/dtmax评估），在心率达到282次/分钟时出现力-频率关系（FFR）下降支，下降支起始于332次/分钟。β-肾上腺素能受体刺激（多巴酚丁胺）使正性FFR向上移位并显著变陡，并使下降支起始时的心率增加到402次/分钟。然后在麻醉恢复期间未起搏的闭胸小鼠（n = 7）中研究心率和LV dP/dtmax，在休息和间歇性体力活动期间，FFR在高达600次/分钟时呈线性且为正性。然后用扎替雷定逐渐减慢心率，休息和活动时的点落在同一条线性关系上。因此我们得出以下结论：1）在开胸麻醉小鼠中，β-肾上腺素能受体刺激放大了正性FFR，并且2）在从麻醉中恢复的小鼠中，窦房结率仍然是心肌收缩力的关键决定因素，没有FFR下降支。
