Effect of stasis of blood in varicose veins on erythrocyte fragility, with accompanying studies comparing red cells and other blood elements with cubital vein blood.

I T HAS been demonstrated by Fahraeus’4 that normal red blood cells have a tendency to bcccme spheroidal in shape after standing in vitro at body ternperature. G#{228}nsslen,5 Haden6 and Castle and Daland7 have shown that spheroidal red cells are more susceptible to osmotic hemolysis than are normal corpuscles. Haden found that normal red cells when suspended in graded hypotonic salt solutions become progressively more globular as the solution becomes more hypotonic, and that there is a direct relationship between the volume thickness index and fragility of the red blood cells. Ham and Castle8 and Tsai, Lee and Wu#{176} have further stated that red cell fragility is increased by stasis of the blood in vitro at body temperature. These investigators found that between one-half and two and one-half hours of stasis was necessary before the first manifestation of increased fragility appeared. Spontaneous hemolysis appeared after approximately twelve hours of stasis. During stasis of blood at body temperature there is also an increase in packed cell volume due to the develo#{231}ment of spheroidal cells.8’ ‘#{176}“ There is also evidence that under some conditicns, in vivo stasis produces increased red cell fragility. Waller12 and Cormick’3 fcuEd an increase in red cell fragility in capillary blood fcllcwing tourni4uet stasis, but Wailer found no increased fragility in blood removed frCm the cubital vein under conditions of stasis except after expressing capillary blood into the veins. There is evidence that concentration and stasis of red blood cells occur normally in the spleen.’1’6 Red cells obtained from the spienic vein were found to be more fragile when suspended in hypotonic salt solutions than red cells from blood in other veins.8’ 9 As further proof that in vivo stasis may cause red cells to become more fragile, Tsai and co-workers9 found that osmotic fragility ofred cells removed from both the splenic and renal veins increased progressively following stasis produced by occlusion of the veins and arteries of the spleen and kidney. Ham and Castle1’ ‘#{176} have attached great importance to the effects of stasis on red cells and consider this factor to be the common denominator in many of the anemias due to hemolysis. They believe that erythrostasis in the spleen is probably the mechanism producing increased blood destruction in the hemolytic anemias with increased red cell fragility, and also, that an unusual degree of erythrostasis might account for some hemolytic anemias in which there is normal or secondarily increased red cell fragility. A number of investigators9 1924 have shown that the red cells usually become less fragile to hypotonic salt solutions