Effects of Norepinephrine on Coronary Circulation and Left Ventricular Dynamics in the Conscious Dog

Effects of Norepinephrine on Coronary Circulation and Left Ventricular Dynamics in the Conscious Dog
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去甲肾上腺素对清醒狗冠状动脉循环和左心室动力学的影响

DOI:
10.1161/01.res.34.6.812
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发表时间:
1974
影响因子:
20.1
通讯作者:
E. Braunwald
E. Braunwald
中科院分区:
医学1区
文献类型:
--
作者:
S. Vatner;C. Higgins;E. Braunwald

文献摘要

被引文献

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本文研究了去甲肾上腺素(0.1和1.0μg/kg,iv)对清醒犬冠脉血流和阻力、左室内压和内径、dp/dt、(dp/dt)/P和心肌纤维缩短速度的影响。当心率保持不变时,去甲肾上腺素引起冠状动脉血管阻力的最初降低,这与平均动脉压、收缩期左室压、舒张末内径、dp/dt、(dp/dt)/P和VISO的增加有关。在短暂的冠状动脉扩张反应后,平均冠状动脉血管阻力持续增加(+0.55±0.07 mm Hg/mlmin−1),平均动脉压(+67±7 mm Hg)、左心室收缩压(+74±6 mm Hg)、左室舒张末压(+4±1 mm Hg)、左心室内径(+1.3±0.3 mm)、峰值dp/dt(+1660 mm Hg/s)、(dp/dt)/P(+15±2 s−1)、VISO(+11±2 mm/s)持续增加;冠状静脉窦血氧分压降低。阻断β受体拮抗去甲肾上腺素的正性肌力作用,减弱早期的冠脉血管扩张作用,增强晚期的血管收缩作用。α受体阻滞剂可消除去甲肾上腺素晚期的冠脉血管收缩作用,仅发生扩张作用。与未阻断自主神经的清醒犬去甲肾上腺素的作用不同,静脉注射去甲肾上腺素(1.0μg/kg,iv)不能引起麻醉开胸犬的晚期冠脉收缩,只有扩张。因此,在正常清醒的狗身上,去甲肾上腺素发挥了一种重要的冠脉血管收缩作用,这种作用足够强烈,足以完全抵消代谢性血管扩张的同时趋势。
The effects of norepinephrine (0.1 and 1.0 μg/kg, iv) on coronary blood flow and resistance, left ventricular pressure and diameter, dP/dt, (dP/dt)/P, and the velocity (VISO) of myocardial fiber shortening were studied in conscious dogs. When the heart rate was held constant, norepinephrine caused an initial reduction in coronary vascular resistance which was associated with increases in mean arterial blood pressure, systolic left ventricular pressure, end-diastolic diameter, dP/dt, (dP/dt)/P, and VISO. After this brief coronary vasodilator response, a sustained increase occurred in mean coronary vascular resistance (+0.55 ± 0.07 mm Hg/ml min−1), and increases persisted in mean arterial blood pressure (+67 ± 7 mm Hg), left ventricular systolic pressure (+74 ± 6 mm Hg), left ventricular end-diastolic pressure (+4 ± 1 mm Hg), left ventricular internal diameter (+1.3 ± 0.3 mm), peak dP/dt (+1660 mm Hg/sec), (dP/dt)/P (+15 ± 2 sec−1), and VISO (+11 ± 2 mm/sec); coronary sinus Po2 decreased. Beta-receptor blockade prevented the inotropic effects of norepinephrine, attenuated the early coronary vasodilator effects, and increased the late vasoconstrictor effects. Alpha-receptor blockade abolished the late coronary vasoconstrictor effects of norepinephrine; only dilatation occurred. In contrast to the effects of norepinephrine in conscious dogs without autonomic blockade , norepinephrine (1.0 μg/kg, iv) failed to produce late coronary vasoconstriction in anesthetized, open-chest dogs; only dilatation occurred. Thus, in the normal, conscious dog, norepinephrine exerts an important coronary vasoconstrictor effect which is sufficiently intense to counteract completely the simultaneous tendency toward metabolic vasodilatation.