The whole blood and corrected blood viscosity of 17 patients with Raynaud's phenomenon (8 with idiopathic Raynaud's phenomenon and 9 with scleroderma-associated Raynaud's phenomenon) have been compared with 12 normal controls. Viscosity has been measured with a Contraves LSV1 rotating viscometer and the Wells-Brookfield microviscometer at 37 degrees C and 25 degrees C and shear rates ranging from 0.775 s-1 to 230 s-1. Blood viscosity was higher at both the lower temperature and the lower shear rates but this change was the same in the patients as in the normal subjects. There was a significantly higher level of plasma fibrinogen in the patients with scleroderma with a significant increase in the corrected blood viscosity, but not the whole blood viscosity, at both temperatures and all shear rates. The percentage increase of viscosity at low temperatures in the patients was the same as the controls. No evidence was found to substantiate the hypothesis that Raynaud's phenomenon is caused by an excessive increase of blood viscosity at low temperatures. Treatment of 10 patients with stanozolol, a stimulator of fibrinolysis, reduced the plasma fibrinogen and increased the haematocrit did not change the whole blood viscosity. Hand blood flow increased. The improvement of hand blood flow was not therefore caused by change in blood viscosity secondary to the reduction of plasma fibrinogen.