Shoukas A A
Circ Res. 1982 Jul;51(1):95-101. doi: 10.1161/01.res.51.1.95.
To quantify the importance of the carotid sinus baroreceptor reflex and the interaction with epinephrine infusion on total pulmonary vascular capacity and resistance, I have simultaneously measured total pulmonary vascular compliance, changes in pulmonary blood volumes, and changes in resistances in seven sodium pentobarbital-anesthetized dogs. A preparation was used that bypasses the right and left hearts allowing for the simultaneous measurement of the pulmonary as well as the systemic vascular bed parameters. At intrasinus pressures of 50, 125, and 200 mm Hg, without epinephrine infusion, the pulmonary vascular resistance was 0.134, 0.121, and 0.109 mm Hg/(ml per min per kg) and the systemic vascular resistance was 1.21, 0.87, and 0.63 mm Hg/(ml per min per kg). Epinephrine infusion of 1 microgram/min per kg at each intrasinus pressure caused the resistances of both vascular beds to increase. Pulmonary vascular resistance increased to 0.157 mm Hg/(ml per min per kg) and showed no further changes with changes in ISP. However, systemic vascular resistance did decrease from 1.49 to 1.41 and 1.25 at intrasinus pressures of 50, 125, and 200 mm Hg. During control runs, pulmonary vascular capacity changed 1.06 ml/kg and systemic capacity changed 7.63 ml/kg for SP changes between 50 and 200 mm Hg. Both responses were greatly attenuated after epinephrine infusion and amounted to only 0.17 ml/kg for the pulmonary and vascular bed and 2.26 ml/kg for the systemic vascular bed. The differences in capacity changes between control and epinephrine runs for the two vascular beds were nearly equal to the change in capacities brought about by epinephrine when it was infused at a fixed intrasinus pressure of 125 mm Hg. The pulmonary vascular compliance during the control runs increased from 0.303 to 0.329 ml/mm Hg per kg when ISP was increased from 50 to 200 mm Hg. After epinephrine infusion, the pulmonary compliance was 0.273 ml/mm Hg per kg and showed no changes with intrasinus pressure. Similar results were obtained for the systemic vascular compliance which was 2.07 ml/mm Hg per kg at an ISP of 50 mm Hg and increased to 2.39 ml/mm Hg per kg to an ISP of 200 mm Hg during control runs. After epinephrine infusion, the systemic compliance was 1.89 ml/mm Hg per kg and again showed no changes with ISP. These data indicate that the baroreceptor reflex can exert control of pulmonary and systemic vascular resistance and capacitance and epinephrine can greatly attenuate the reflex control of both vascular beds.
为了量化颈动脉窦压力感受器反射的重要性以及肾上腺素输注对总肺血管容量和阻力的影响,我同时测量了7只戊巴比妥钠麻醉犬的总肺血管顺应性、肺血容量变化和阻力变化。采用了一种绕过左右心脏的制备方法,以便同时测量肺血管床和体循环血管床的参数。在窦内压力为50、125和200 mmHg时,未输注肾上腺素,肺血管阻力分别为0.134、0.121和0.109 mmHg/(每千克每分钟毫升),体循环血管阻力分别为1.21、0.87和0.63 mmHg/(每千克每分钟毫升)。在每个窦内压力下以1微克/(每千克每分钟)的速率输注肾上腺素导致两个血管床的阻力均增加。肺血管阻力增加到0.157 mmHg/(每千克每分钟毫升),并且随着窦内压力的变化没有进一步变化。然而,在窦内压力为50、125和200 mmHg时,体循环血管阻力确实从1.49降至1.41和1.25。在对照实验中,当窦内压力在50至200 mmHg之间变化时,肺血管容量变化为1.06毫升/千克,体循环容量变化为7.63毫升/千克。输注肾上腺素后,两种反应均显著减弱,肺血管床仅为0.17毫升/千克,体循环血管床为2.26毫升/千克。两个血管床在对照和肾上腺素输注实验中容量变化的差异几乎等于在125 mmHg的固定窦内压力下输注肾上腺素所引起的容量变化。在对照实验中,当窦内压力从50 mmHg增加到200 mmHg时,肺血管顺应性从0.303增加到0.329毫升/(每千克每毫米汞柱)。输注肾上腺素后,肺顺应性为0.273毫升/(每千克每毫米汞柱),并且随着窦内压力的变化没有变化。体循环血管顺应性也得到了类似的结果,在窦内压力为50 mmHg时为2.07毫升/(每千克每毫米汞柱),在对照实验中当窦内压力增加到200 mmHg时增加到2.39毫升/(每千克每毫米汞柱)。输注肾上腺素后,体循环顺应性为1.89毫升/(每千克每毫米汞柱),同样随着窦内压力的变化没有变化。这些数据表明,压力感受器反射可以对肺血管和体循环血管的阻力及容量进行控制,而肾上腺素可以极大地减弱对两个血管床的反射控制。