Hiser W, Penman R W, Reeves J T
Am Rev Respir Dis. 1975 Dec;112(6):817-22. doi: 10.1164/arrd.1975.112.6.817.
To determine the role of hypoxic pulmonary vasoconstriction in pneumococcal pneumonia, hemodynamic measurements were made in 16 dogs before, and within 36 hours after, intrapulmonary administration of type III pneumococcus. Ten dogs with one lobe or more of pneumonia increased their pulmonary vascular resistances and slightly decreased their arterial O2 tensions. Hypoxia increased and hyperoxia decreased their pulmonary vascular resistances. During O2 breathing, arterial PO2 was less during than before the pneumonia and increased when pulmonary perfusion was diverted away from the diseased lung. In 2 dogs breathing air, forcing the cardiac output through the diseased lung caused an increase in vascular resistance that could clearly be reduced by O2 breathing. In 5 dogs, lung mast cell counts showed no decrease in the lobes with pneumonia. In pneumococcal pneumonia, the hypoxic pulmonary pressor mechanism serves to decrease blood flow to the diseased lobes and, thus, to maintain the arterial PO2. Lung mast cells could participate in this response.
为了确定低氧性肺血管收缩在肺炎球菌肺炎中的作用，对16只狗在肺内注射Ⅲ型肺炎球菌之前及之后36小时内进行了血流动力学测量。10只患有一个或多个肺叶肺炎的狗增加了肺血管阻力，并使动脉血氧张力略有下降。低氧使肺血管阻力增加，高氧则使其降低。在吸氧过程中，动脉血氧分压在肺炎期间低于肺炎前，当肺灌注从患病肺叶转移时则升高。在2只呼吸空气的狗中，迫使心输出量通过患病肺叶会导致血管阻力增加，而吸氧可明显降低这种阻力。在5只狗中，肺叶肺炎部位的肺肥大细胞计数没有减少。在肺炎球菌肺炎中，低氧性肺升压机制有助于减少流向患病肺叶的血流，从而维持动脉血氧分压。肺肥大细胞可能参与了这一反应。
