Olson N C, Robinson N E, Scott J B
J Surg Res. 1983 Jul;35(1):21-7. doi: 10.1016/0022-4804(83)90121-x.
The effects of acute brain hypoxia on pulmonary hemodynamics were investigated in anesthetized dogs with the vagus and carotid sinus nerves intact and cut. Following ligation of collateral vessels, brain hypoxia was induced by pumping arterial blood through a ventilated extracorporeal lung to the external carotid arteries for 5 min. In the intact-nerve group brain hypoxia caused no change in pulmonary and systemic vascular pressures and resistances. In the cut-nerve group brain hypoxia caused an increase in mean pulmonary artery, left atrial, pulmonary artery pulse, and mean aortic pressures. Cardiac output, dP/dt, central blood volume, and total peripheral resistance increased but pulmonary vascular resistance and lung extravascular thermal volume were unchanged. It is concluded that acute brain hypoxia does not increase pulmonary vascular resistance but may increase pulmonary blood volume resulting from increased left ventricular afterload.
在迷走神经和颈动脉窦神经完整及切断的麻醉犬中,研究了急性脑缺氧对肺血流动力学的影响。在结扎侧支血管后,通过将动脉血经体外通气肺泵入颈外动脉5分钟来诱导脑缺氧。在神经完整组中,脑缺氧对肺和体循环血管压力及阻力无影响。在神经切断组中,脑缺氧导致平均肺动脉压、左心房压、肺动脉脉搏压和平均主动脉压升高。心输出量、dp/dt、中心血容量和总外周阻力增加,但肺血管阻力和肺血管外热容量未改变。得出的结论是,急性脑缺氧不会增加肺血管阻力,但可能因左心室后负荷增加导致肺血容量增加。