Hemolytic Anemia In Dogs Research Articles

Pirimicarb induced immune haemolytic anaemia in dogs.

The feeding of pirimicarb (2-dimethylamino-5,6-dimethylpyrimidin-4-yl dimethylcarbamate) to normal beagle dogs resulted in anaemia in a small number of animals. Dosing studies confirmed pirimicarb as the causative agent and the anaemia was characterised as haemolytic. Serological tests revealed the presence of an IgG antibody active only in the presence of pirimicarb. The level of antibody detected was related to the dose of pririmicarb given.

玉葱の給与による犬の急性溶血性貧血症の発生例について

玉葱の給与による犬の急性溶血性貧血症の発生例について

Hemoglobin concentration overestimates oxygen carrying capacity of blood in phenylhydrazine-induced hemolytic anemia in dogs.

Acute hemolytic anemia in patients with red blood cells deficient in enzymes such as G-6-PD is characterized by excessive oxidation of hemoglobin (Hb) to a variety of soluble heme pigments and to precipitates, attached to the inner surface of the red cell membrane, known as Heinz bodies (1). These pigments and precipitates do not carry oxygen. The cyanmethemoglobin method. widely used to determine blood Hb concentration, detects not only Hb but methemoglobin and other non-oxygen carrying heme pigments as well; sulfhemoglobin is not detected by this method (2). The present study tested the hypothesis that non-oxygen carrying pigments might constitute a significant fraction of “hemoglobin,” as measured by the cyanmethemoglobin method, during the course of acute hemolytic anemia induced in dogs by phenlyhydrazine, a potent oxidizing agent. Measured blood oxygen carrying capacity (CmaxO2) was less than the CmaxO2 expected from Hb in anemic dogs. The data thus confirm the hypothesis. Additional studies indicat...

Morphologic effects of minocycline in laboratory animals

The morphologic effects of minocycline were studied in rats, dogs, monkeys, and mice using various routes of drug administration and graded doses. The results of these short-term studies ranging from 27 to 38 days can be summarized as follows: Minocycline caused various degrees of hemolytic anemia in dogs after the intravenous infusion of 10–40 mg/kg/day for 27–29 days, but not after 5 mg/kg/day. After one month, a black discoloration of the thyroid glands was found in monkeys (30 mg/kg/day; orally), dogs (40, 20, 10, and 5 mg/kg/day; intravenously), rats (75, 25, and 8 mg/kg/day; orally), but not in mice (250 mg/kg/day; orally). Rats and dogs showed a deposition of pigment in the thyroid glands sometimes associated with hyperplastic changes. In the canine species this hyperplasia was associated with the formation of thyroidectomy cells in the pituitary gland after the administration of 40 and 20 mg/kg/day of minocycline intravenously for 27–29 days. The pigmentation was much less pronounced in monkeys than in any other species. No hyperplastic changes were noticeable. Electron microscopic observations and special staining procedures indicated that the nonfluorescent pigment was formed within the intraepithelial colloid droplets. The simultaneous administration of propylthiouracil plus minocycline or thyroid powder USP plus minocycline to rats caused morphologic activation or hyperplastic changes phase phenomena, respectively, without pigmentation of the thyroid glands. These findings indicate that oxidative enzyme activity (presumably absent in flat thyroid epithelium associated with the storage phase or blocked by propylthiouracil) is necessary for the deposition of pigment. The pigment was still present in thyroid glands of rats that received 75 mg/kg/day for 38 days and were then kept for one year on a normal diet. No other changes were seen at this time. The oral administration of minocycline caused yellow discoloration of femora and skulls without any deleterious effect on bone growth.

ON THE ORIGIN OF CERTAIN SERUM PEPTIDASES AS INDICATED BY EXPERIMENTAL HEMOLYTIC ANEMIA IN DOGS

ON THE ORIGIN OF CERTAIN SERUM PEPTIDASES AS INDICATED BY EXPERIMENTAL HEMOLYTIC ANEMIA IN DOGS