Anemia plays a major role in myocardial hypertrophy of copper deficiency.
The present study was undertaken to establish whether anemia plays a role in the cardiomegaly and myocardial pathology of copper deficiency. Fifteen weanling male rats were fed a copper-deficient (0.6 microgram Cu/g) diet for 5 weeks. Six rats were intraperitoneally injected once a week with packed red blood cells (RBC) that were obtained from copper-deficient rats fed starch. The remainder (n = 9) served as controls. The administration of RBC to copper-deficient rats fed fructose prevented the anemia. As a result, none of the injected rats exhibited heart hypertrophy or gross pathology and they all survived. In contrast, all other control, nontreated copper-deficient rats that were fed fructose were anemic and all exhibited severe signs of copper deficiency, which included heart hypertrophy with gross pathology, and four died of the deficiency. The data suggest that the anemia of copper deficiency contributes to heart pathology. Once the anemia is prevented, the copper-deficient rats should be protected against heart pathology and mortality.
Fields
M
M
Division of Endocrinology, Georgetown University Medical School, Washington, DC.
Lewis
C G
CG
Lure
M D
MD
D000740:Anemia / Q000503:physiopathology* / Q000517:prevention & control; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology; D003300:Copper / Q000172:deficiency*; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D005632:Fructose / Q000008:administration & dosage / Q000627:therapeutic use; D008297:Male; D009206:Myocardium / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains
D004040:Dietary Carbohydrates; D005632:Fructose; D003300:Copper