Dowell R T, Houdi A A
Lake Erie College of Osteopathic Medicine, Pennsylvania, USA.
Methods Find Exp Clin Pharmacol. 1997 Oct;19(8):533-9.
The present studies were conducted in conscious, instrumented rats to evaluate measurements of aortic peak flow velocity (PFV) as an index of myocardial contractility. Because our previous studies had characterized/verified procedures to determine pressure-derived indices of contractile function in the anesthetized, ventilated, open-chest rat, we first correlated PFV with (a) maximum rate of left ventricular pressure development (max +dP/dt) and (b) a contractility index derived by dividing max +dP/dt by left ventricular pressure at max +dP/dt [(dP/dt)/P] in anesthetized rats (n = 5). The positive inotropic agent, isoproterenol, given by bolus intravenous injection (0.2 microgram), significantly and concurrently increased dP/dt, (dP/dt)/P, and PFV. The negative inotropic agent, propranolol, given by bolus intravenous injection (2 mg/kg), significantly and concurrently attenuated all of the above measurements. When control, isoproterenol, and propranolol responses were used to calculate multivariate correlation coefficients among dP/dt, (dP/dt)/P, and PFV, r values ranged from 0.74 (PFV vs. dP/dt) to 0.84 (dP/dt vs. (dP/dt)/P) to 0.91 (PFV vs. (dP/dt)/P). A separate group of rats (n = 4) was surgically implanted with ascending aortic blood flow sensors, carotid artery and jugular vein catheters. Intravenous isoproterenol (0.2 microgram, bolus) elicited increased cardiac (heart rate and cardiac output) and decreased peripheral vascular resistance (mean arterial blood pressure) beta-adrenergic receptor agonist effects. Propranolol (2 mg/kg, i.v. bolus) produced hemodynamic effects consistent with cardiovascular beta-adrenergic receptor blockade. Isoproterenol and propranolol had directionally appropriate, and significant effects on PFV in the conscious rat. When compared with PFV values under control conditions in the anesthetized rat, conscious rat values are approximately double those observed under anesthesia; however, the relative PFV responses to isoproterenol and propranolol were not affected. Therefore, the present studies provide evidence that aortic PFV can be utilized as an estimate of heart contractile performance, i.e., myocardial contractility, in the conscious, instrumented rat.
本研究在清醒、植入仪器的大鼠身上进行,以评估主动脉峰值流速(PFV)测量值作为心肌收缩力指标的情况。由于我们之前的研究已对在麻醉、通气、开胸大鼠中确定收缩功能压力衍生指标的程序进行了表征/验证,我们首先在麻醉大鼠(n = 5)中将PFV与(a)左心室压力最大上升速率(max +dP/dt)以及(b)通过将max +dP/dt除以max +dP/dt时的左心室压力得出的收缩力指标[(dP/dt)/P]进行关联。通过静脉推注给予正性肌力药物异丙肾上腺素(0.2微克),显著且同时增加了dP/dt、(dP/dt)/P和PFV。通过静脉推注给予负性肌力药物普萘洛尔(2毫克/千克),显著且同时减弱了上述所有测量值。当使用对照、异丙肾上腺素和普萘洛尔反应来计算dP/dt、(dP/dt)/P和PFV之间的多元相关系数时,r值范围从0.74(PFV与dP/dt)到0.84(dP/dt与(dP/dt)/P)再到0.91(PFV与(dP/dt)/P)。另一组大鼠(n = 4)通过手术植入升主动脉血流传感器、颈动脉和颈静脉导管。静脉注射异丙肾上腺素(0.2微克,推注)引发心脏(心率和心输出量)增加以及外周血管阻力(平均动脉血压)降低的β-肾上腺素能受体激动剂效应。普萘洛尔(2毫克/千克,静脉推注)产生与心血管β-肾上腺素能受体阻断一致的血流动力学效应。异丙肾上腺素和普萘洛尔对清醒大鼠的PFV有方向合适且显著的影响。与麻醉大鼠对照条件下的PFV值相比,清醒大鼠的值约为麻醉下观察值的两倍;然而,PFV对异丙肾上腺素和普萘洛尔的相对反应未受影响。因此,本研究提供了证据表明主动脉PFV可被用作清醒、植入仪器大鼠心脏收缩性能即心肌收缩力的估计指标。