Eight ponies were allotted to 2 groups of 4. Group-1 ponies (1-4) were given 0.2 g of indole/kg of body weight orally and group-2 ponies (5 to 8) were given 0.1 g of indole/kg. Various physical, hematologic, and physiologic measurements were obtained after administration of indole. Intravascular hemolysis and hemoglobinuria were detected in both groups within 24 hours of dosing. Hemolysis was reflected by decreases in PCV, hemoglobin concentration, and RBC count, and an increase in indirect bilirubin. Erythrocyte fragility appeared to increase in both groups at 8 hours after dosing and peaked at 16 hours after dosing. At 72 hours after dosing, the RBC fragility value was less than predose measurements. Heinz body formation was noticed in group-2 ponies, but not in group 1. Plasma indole concentrations increased in both groups from the nondetectable predose concentrations. Group-1 values were 203% of group-2 values. In group 2, plasma indole was nondetectable by 12 hours, whereas low concentrations could still be measured in the group-1 ponies at 24 hours. Ponies in group 1 died or were euthanatized between 24 and 72 hours after dosing, whereas group-2 ponies were euthanatized between 48 and 120 hours. At necropsy, all body fat, mucous membranes, and elastic tissue were stained yellow. Hemoglobinuric nephrosis was the most prominent microscopic lesion. Results of this study indicated that indole, a metabolite of the amino acid tryptophan, causes acute intravascular hemolysis in ponies.

Iron status, as determined by hematologic values, serum iron concentration, total iron-binding capacity, and zinc protoporphyrin concentration, was determined in 2 groups of 6 nonpregnant monkeys. Monkeys of groups 1 and 2 had 10 and 5%, respectively, of their blood volume withdrawn per week for up to 10 weeks or until blood hemoglobin concentration was less than or equal to 10 g/dl. A third group of 6 monkeys served as controls. The majority (8/12) of the monkeys became anemic (hemoglobin concentration, less than or equal to 10 g/dl) after approximately 30 to 70% (mean, 49%) of their blood volume was removed. Anemia was accompanied by decrease in serum iron concentration and percentage of transferrin saturation. Microcytosis, hypochromasia, and increased zinc protoporphyrin concentration, all hematologic characteristics of iron deficiency, developed later. The calculated iron stores ranged from 1 to 133 mg, with mean value of 51 mg. Iron-depleted monkeys had mean calculated available iron store of 20.8 mg, whereas iron-replete monkeys had mean available iron store of 114.0 mg. Changes were not observed in monkeys of the control group during the study period. None of the baseline hematologic or biochemical analytes measured were good predictors of iron stores. The diet used at the research center did not provide sufficient iron to prevent iron deficiency in most of the monkeys from which a total amount of 30 to 70% of blood volume at 5 or 10%/week was withdrawn. Studies requiring that much blood may need to be modified to include iron supplementation, reduction of sample volume, or iron replacement after termination of projects.