Studies of peripheral circulation during sickle-cell crisis.

IT IS WELL recognized that patients with sickle-cell disease may have a low saturation and tension of arterial blood oxygen. Although arterial anioxemia was first observed in 1942, its exact mechanism is still unknown.1 It has been shown that the hemoglobin dissociation curve of these patients is shifted to the right, probably because of a decrease in erythrocyte pH.2, 3 Therefore, a norimal level of oxygen saturation would not be possible even in the preselnce of a normal oxygen tension. A block of diffusion at alveolar-capillary membrane resulting in an inereased pressure gradient of alveolar-arterial oxygen has also been suggested as a cause of arterial oxygen unsaturation.4 It appears more likely, however, that abnormal venous admixture within the lungs, as reported in other anemias,5 is responsible for a low arterial oxygen tension.6 Congenital abnormalities in the lunig vasculature, opening of pulmnonary arteriovenious anastomotic channels, extremely low oxygen tension in the returning venous blood, or pulmonary parenchymal alterations have been suggested as mechanisms by which abnormal venous admixture within the lungs occurs.6 Apparently, shunting of blood within the lungs accounts for the arterial oxygen unsaturation observed in sickle-cell disease. The possibility that abnormal shunts are also present in the peripheral circulation of these patients has not been investigated, although it has been recently suggested in the results of experiments intended to show abnormal intrapulmonarv venous admixture.6 The present study was undertaken to investi-