Key points are not available for this paper at this time.
To quantify the interaction between epinephrine infusion and carotid sinus baroreceptor reflex control of vascular capacity and resistance, we have simultaneously measured total systemic compliance, C t , arterial compliance, C a , changes in "unstressed vascular volume," AV 0 , and resistance, R, in nine dogs whose carotid sinuses were isolated and cardiac output fixed by a perfusion pump. In response to intrasinus pressures (ISP) of 50, 125, and 200 mm Hg without epinephrine infusion, total systemic compliance (C t ) was 1.00, and 1.10, and 1.22 ml/mm Hg per kg, whereas arterial compliance showed no change and averaged 0.0984 ml/mm Hg per kg for all ISP's. Resistance was 1.45, 0.88, and 0.57 nun Hg/(ml per min per kg) for intrasinus pressure of 50, 125, and 200 mm Hg. The change in unstressed vascular volume from ISP of 50 to 125 was 7.32 ml/kg and 5.03 ml/kg for an ISP change from 125 to 200 mm Hg. When epinephrine was infused at a constant rate of 1.2 /ig/min per kg at a fixed ISP of 125 mm Hg, arterial pressure rose by 69.1 mm Hg, the change in unstressed vascular volume was 8.02 ml/kg, and resistance increased from 0.89 to 1.54 mm Hg/(ml per min per kg), an increase of 73% of control. At the same infusion rate and at each ISP of 50, 125, and 200 mm Hg, compliances, C t and C, and resistance were measured. In contrast to the control data, C t showed no increase with changes in ISP (0.92, 0.94, and 0.92 ml/mm Hg per kg), whereas C, measured 0.081 ml/ mm Hg per kg. Resistance was 1.71, 1.46, and 1.19 mm Hg/min per kg for intrasinus pressures of 50, 125, and 200 mm Hg. The change in unstressed vascular volume caused by an ISP change of 50-125 mm Hg was 1.78 ml/kg and for an ISP change of 125-200 mm Hg was 1.30 ml/kg. The data indicate that epinephrine greatly attenuates the reflex control of the vascular properties by mechanisms other than the modification of the carotid sinus receptor characteristics. Circ Res 47: 249250251252253254255256257 1980 THE pressor action of epinephrine is well documented in most textbooks of physiology. However, most of the studies on epinephrine have used isolated parts of the circulation. Difficulty arises when one attempts to quantify the contributions of these various parts to the overall pressor effect of epinephrine Although these studies dealt with the quantitative effects of epinephrine on the capacitive and resistive properties of the systemic vascular bed, the carotid sinus and aortic arch baroreceptor regions were not denervated, and the pressures in these receptor areas were not controlled. Thus, the apparent actions of epinephrine could have been buffered by the carotid sinus baroreceptor reflex which has been shown to change
Shoukas et al. (Fri,) studied this question.