Abstract
A decrease in blood viscosity, caused by the intravenous injection of sodium tetrathionate, has been reported by Theis and Freeland (1). This decrease apparently is accompanied by an increase in oxygen saturation. The pathogenesis of sickle cell anemia, while yet obscure, seems to be associated, according to Pauling, et al. (2) with an abnormality in the structure of the hemoglobin molecule. This abnormality is reflected by changes in the shape of the erythrocyte, under reduced oxygen tension, which cause an increase in blood viscosity, thus setting up a vicious cycle, which may terminate in a state of crisis. The purpose of this investigation was to determine whether sodium tetrathionate would break the above mentioned vicious cycle by decreasing the viscosity of the blood of sickle cell anemia patients.
It has been shown(3) that by using an Ostwald type viscosimeter the relative viscosity of blood samples, after exposure to oxygen and carbon dioxide, can be expressed in seconds and that the difference, expressed in seconds, should be a fairly accurate measure of the viscousness of the blood of a patient with sickle cell anemia in crises. Simple measurements of absolute viscosity were deemed unsatisfactory in that changes in protein concentration or water balance, hemolysis or peptization of serum proteins would make the evaluation of results difficult. The use of the “difference value” simply uses the oxygenated blood as a control and thus eliminates, to a great extent, factors other than those pertaining to the erythrocyte itself.
Twelve patients, with definitely proved sickle cell anemia in crisis, or seemingly approaching crisis, were given sodium tetrathionate† by vein. Relative viscosity under carbon dioxide and oxygen, hemoglobin, and serum protein determinations were made, before and after the drug, upon a number of successive days.
Get full access to this article
View all access options for this article.