THE RELATION OF THE SPLEEN TO BLOOD DESTRUCTION AND REGENERATION AND TO HEMOLYTIC JAUNDICE : XV. THE RESISTANCE TO HEMOLYTIC AGENTS OF DOGS IN WHICH THE SPLENIC BLOOD HAS BEEN DIVERTED FROM THE LIVER.

Abstract

1. Dogs whose splenic veins or portal vein (Eck fistula) have been transplanted into the inferior vena cava, or whose splenic veins have been ligated, show a lessened tendency to jaundice similar to that exhibited by splenectomized animals. 2. Although the previously existing anemia and the concomitant increased resistance of the red cells of these animals are undoubtedly factors in the greater resistance to hemolytic agents, the lessened tendency to jaundice is, in part at least, due to a mechanical factor dependent on the course of the blood supply to the liver. 3. The additional anemia caused in the test animals by hemolytic agents is usually less than in the controls, although the total fall from the original normal may be greater. This applies to the splenectomized as well as the other test animals and is a modification of our former statements in regard to the severity of the anemia in splenectomized dogs. 4. Although the destruction of blood in these animals is less than in the normal controls, the repair of the same takes considerably longer than in the controls. This confirms similar results previously obtained in splenectomized animals. 5. The white cells exhibit much the same changes as they do following the administration of hemolytic agents to splenectomized or normal animals. As these changes are not unlike those following uncomplicated splenectomy or the operations here discussed, they cannot be considered as characteristic of any of the above procedures, but perhaps as an accompaniment of any temporary increased blood destruction. 6. The reaction of test and control animals is substantially the same, whether the jaundice is caused by toluylenediamin or hemolytic immune serum.

• Authors: E B Krumbhaar, J H Musser
• Journal: The Journal of experimental medicine (J Exp Med) Vol. 23 Issue 1 Pg. 97-106 (Jan 01 1916) ISSN: 0022-1007 [Print] United States
• PMID: 19867974 (Publication Type: Journal Article)