Genovesi M G, Tierney D F, Taplin G V, Eisenberg H
Am Rev Respir Dis. 1976 Jul;114(1):59-65. doi: 10.1164/arrd.1976.114.1.59.
Using conventional concepts, it is possible that a single pathologic entity, pulmonary telangiectases, can produce hypoxia by 3 physiologic mechanisms; shunt, diffusion defect, and ventilation-perfusion abnormalities. The estimation of shunt or shunt-like effect is traditionally calculated by measuring the Po2 of arterial blood during the breathing of 100 per cent 02. This method, however, did not determine blood flow through large alveolar vessels in a patient with familial hemorrhagic telangiectasis who was severely hypoxemic while breathing air. This case served to test the concept that blood flowing through large vessels in the airspaces may be hypoxemic when the patient breathes air, but not 02. Blood flow through these vessles can be estimated by use of radionuclide lung perfusion techniques and estimation of the quantity of radioactive particles that pass through an abnormal pulmonary vascular bed and lodge in kidney and brain. Conventional approaches to estimating blood flow through these fistulas underestimated their effect.
按照传统观念，单一病理实体——肺毛细血管扩张症有可能通过三种生理机制导致缺氧，即分流、弥散障碍和通气-灌注异常。传统上，分流或类分流效应的评估是通过在吸入100%氧气时测量动脉血氧分压来计算的。然而，这种方法无法测定患有家族性出血性毛细血管扩张症且在呼吸空气时严重低氧血症患者的大肺泡血管中的血流情况。该病例用于检验这样一种概念，即在患者呼吸空气而非氧气时，气腔内大血管中的血流可能是低氧的。通过使用放射性核素肺灌注技术以及估算通过异常肺血管床并滞留于肾脏和大脑中的放射性粒子数量，可以估计这些血管中的血流。传统的估算这些瘘管中血流的方法低估了它们的影响。
