Furuya M E, Ramírez J C, Maxwell R, Sandoval J, Lupi-Herrera E
Servicio de Cardioneumología, Instituto Nacional de Cardiología Ignacio Chávez, México, D.F.
Arch Inst Cardiol Mex. 1988 Jan-Feb;58(1):5-9.
In order to evaluate the isolated hemodynamic effects of acute hypercapnea on pulmonary circulation, we designed a canine model in which vascular pressures. PaO2, and arterial pH were maintained within normal limits. Six mongrel dogs were studied. Hypercapnea was achieved by a single intravenous doses of acetazolamide (120 mg/Kg) while maintaining mechanical ventilation constant. Both arterial and mixed venous PCO2 increased from 27 to 41 mm Hg and from 31 to 46 mm Hg respectively, and remained constant through the rest of the experiment (up to 3 Hs). With hypercapnea, total pulmonary vascular resistance increased from 312 +/- 156 to 435 +/- 173 d.s.cm-5 (p less than 0.05) and the stroke index decreased from 20.7 +/- 8.3 to 13.2 +/- 4.8 ml/beat (p less than 0.05). There were no changes either in pulmonary capillary wedge pressure or in the right ventricular end diastolic pressure. The above changes suggest a pulmonary vasoconstrictor effect of hypercapnea in the absence of other known vasoactive factors.
为了评估急性高碳酸血症对肺循环的孤立血流动力学效应，我们设计了一种犬类模型，其中血管压力、动脉血氧分压（PaO2）和动脉血pH值维持在正常范围内。研究了6只杂种犬。通过单次静脉注射乙酰唑胺（120mg/kg）实现高碳酸血症，同时保持机械通气不变。动脉血和混合静脉血二氧化碳分压（PCO2）分别从27mmHg升至41mmHg和从31mmHg升至46mmHg，并在实验剩余时间（长达3小时）内保持恒定。出现高碳酸血症时，总肺血管阻力从312±156dyn·s/cm⁵增至435±173dyn·s/cm⁵（p<0.05），每搏输出指数从20.7±8.3ml/次降至13.2±4.8ml/次（p<0.05）。肺毛细血管楔压和右心室舒张末期压力均无变化。上述变化表明，在不存在其他已知血管活性因子的情况下，高碳酸血症具有肺血管收缩作用。
