In veterinary medicine, PCV determined by centrifugation of blood in a microhematocrit tube is the most common clinical test used to initially assess and monitor anemic and polycythemic animals. In contrast, blood hemoglobin (Hb) concentration, rather than PCV, is generally determined in human patients. One automated system photometrically measures blood Hb concentration after conversion of Hb to azide methemoglobin without dilution and was found to be a simple and accurate instrument for use in human medicine. We evaluated the system for its accuracy in measuring blood Hb concentration in animals by comparing it with standard techniques and for its suitability in veterinary practice. Blood samples, anticoagulated with potassium EDTA, from 78 healthy animals (33 dogs, 17 cats, 13 horses, and 15 cows) and 58 dogs and 4 cats with various blood abnormalities (10 anemia, 11 polycythemia, 21 lipemia, 16 leukocytosis, and 6 icterus) were analyzed. In all species, blood Hb concentration of healthy animals determined by the system was comparable to that measured by standard cyanmethemoglobin methods (ie, an automated counter; rI = 0.987 to 0.998 and a hemoglobin kit, rI = 0.946 to 0.993). The aforementioned system also yielded similar values to those obtained by use of standard methods in anemic, polycythemic, and icteric dogs and cats. Moreover, the system reads the absorbance at 2 wavelengths to correct for turbidity, and therefore, accurately measured Hb concentration in blood samples with severe lipemia (triglycerides concentration > 500 mg/dl) and marked leukocytosis (> 50,000 WBC/microl), whereas other standard Hb techniques are known to give falsely high results. We conclude that the automated system compares favorably to standard methods, and is a simple and accurate instrument to quickly measure Hb concentration in animals.

Magnesium (Mg2+) plays an important role in the regulation of a range of intracellular processes. Regulation of extracellular Mg2+ contents was studied in the anesthetized Sprague-Dwley (SD) rats. Animals were injected intraperitoneally with sodium nitrite (NaNO2), and circulating Mg2+([Mg2+]c) was observed in animals injected with NaNO2 at a dose of 10mg/kg or higher. Pretreatment with methylene blue preventd the NaNO2-induced increse in [Mg2+]c.[Mg2+]c displayed an inverse linear correlation with hemoglobin and exponential correlation during NaNO2 injection. Injection of KCN or rotenone also induced an increase in [Mg2+]c. An increase in [Mg2+]c was observed when respiration rate was reduced from 100/min (140ml/min) to 10/min (14ml/min) during 30 min. These results indicate that changes in [Mg2_]c inversely reflect alteration of ATP in a model of metabolic inhibition

alpha-Hemoglobin stabilizing protein (AHSP) functions as the erythroid-specific molecular chaperon for alpha-globin. AHSP gene expression has been reported to be downregulated in hematopoietic tissues of animals suffering from prion diseases though the mechanism remains to be clarified. Herein, we demonstrate that MELhipod8 cells, a subclone of murine erythroleukemia (MEL) cells, have prion protein (PrPsup(C)) on the cell surface and have highly inducible expression of the AHSP and alpha- and beta-globin genes, resembling the expression pattern of the PrP and AHSP genes in bipotential erythroid- and megakaryocyte-lineage cells followed by erythroid differentiation in normal erythropoiesis. Moreover, MELhipod8 cells exhibit greater effective erythroid differentiation with a population of hemoglobinized normoblast-like cells than that observed for the parental MEL cells. These findings suggest that MELhipod8 cells could provide a mechanism for downregulation of the AHSP gene in prion diseases.

The phenotypes of hemoglobin, albumin and transferrin of 302 Jindo dogs in Jindo area were studied by starch gel electrophoresis for hemoglobin and albumin, and by polyacrylamide gradient gel electrophoresis for transferrin. In the hemoglobin phenotypes, three phenotypes, HbAA, HbAB and HbBB, which were controlled by two allelic genes, Hb** (A) and Hb** (B), were observed and their frequencies of appearance were 1.65%, 10.60% and 87.75% respectively. The distribution of gene frequency was calculated as 0.0695 in Hb** (A) and 0.9305 in Hb** (B). In the albumin phenotypes, three phenotypes, Alb FF, Alb FS and Alb SS, which were controlled by two allelic genes, Alb** (F) and Alb** (S) were observed and their frequencies of appearance were 12.59%, 25.56% and 61.85% respectively. The distribution of gene frequency was calculated as 0.2537 in Alb** (F) and 0.7463 in Alb** (S). Analysis of transferrin phenotypes showed 6 different types which were controlled by three allelic genes, Tf** (B), Tf** (C) and Tf** (D), and their frequencies of appearance were 54.04% in TfBB, 17.54% in TfBC, 9.82% in TfBD, 8.07% in TfCC, 7.37% in TfCD and 3.16% in TfDD. The distribution of gene frequency was calculated as 0.6772 in Tf** (B), 0.2053 in Tf** (C) and 0.1175 in Tf** (D)