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- Author or Editor: Russell L. Tucker x
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Abstract
Objective
To determine posttransfusion viability (PTV) of canine RBC stored for 35 days in an additive solution, using in vitro biotinylation and technetium-99m and chromium-51 (99mTc/51Cr) labeling techniques.
Sample Population
6 random source, adult dogs.
Procedure
RBC from dogs were labeled with N-hydroxysuccinimide biotin (NHS-biotin) or 99mTc/51Cr in a crossover design. One unit (450 ml) of whole blood was collected from each dog, processed into packed RBC, and stored for 35 days in an additive solution. The process was repeated at a later date, so that each dog had 2 units stored under similar conditions. Stored autologous RBC were then labeled with either NHS-biotin or 51Cr and reinfused. When 51Cr was used, labeled cells were infused simultaneously with freshly drawn cells labeled with 99mTc. Posttransfusion viability of labeled cells was determined by dividing counts per minute (99mTc/51Cr) or percentage of cells (NHS-biotin) labeled at 24 hours by counts per minute or percentage of cells labeled after infusion.
Results
Mean PTV of packed RBC stored for 35 days in an additive system was 80% when determined by biotinylation, 83% as determined by 99mTc/51Cr, and 81% as determined by 51Cr alone.
Conclusions
In vitro biotinylation provides an acceptable, nonradioisotopic means of determining PTV of stored canine packed RBC.
Clinical Relevance
NHS-biotin can be used to determine maximal storage time of canine RBC prepared for transfusion purposes. (Am J Vet Res 1998;59:397–400)
Summary
Isolated equine granulocytes (wbc), radiolabeled with 99mTc-hexamethylpropyleneamine oxime (99mTc-hmpao) or 111In-oxine, were evaluated in vitro for their labeling characteristics, viability, and phagocytic function over a 6-hour postlabeling period. Mean ± sd labeling efficiency for 111In-oxine-wbc was 62.2 ± 15.3%, which was significantly (P < 0.001) higher than that for 99mTc-hmpao-wbc (32.0 ± 17.0%). In vitro elution of radiolabel from cells was significantly (P < 0.02) greater for 99mTc-hmpao-wbc at 0.5, 2, and 4 hours, but was not significantly different from elution of radiolabel for 111In-oxine-wbc at 6 hours. Viability, assessed by trypan blue dye exclusion, for 99mTc-hmpao-wbc, 111In-oxine-wbc, and nonlabeled control wbc ranged from 97 to 100%, and was not significantly different among groups. Cell function was assessed by use of a phagocytosis assay and was reported as phagocytic index. The phagocytic index ranged from 0.86 to 0.96 for 99mTc-hmpao-wbc, and from 0.76 to 0.97 for 111In-oxine-wbc. The phagocytic index was not significantly different at 0.5, 2, or 4 hours, but was significantly (P = 0.038) greater at 6 hours for 99mTc-hmpao-wbc. Because of the superior imaging characteristics of 99mTc-hmpao-wbc and equal or better labeling characteristics than those for 111In-oxine at 6 hours, 99mTc-hmpao-wbc appear to be a good alternative to 111In-oxine-wbc.
Abstract
Objective—To determine whether the reported drug-drug interaction between the flea medication spinosad and ivermectin is attributable to inhibition of P-glycoprotein by spinosad.
Animals—6 healthy adult dogs with the ABCB1 wildtype genotype.
Procedures—The study was conducted as a prospective, masked, randomized crossover design. Six dogs were allocated to 2 groups; each dog served as its own control animal. Dogs in one of the groups received spinosad at the manufacturer's recommended dose; the other group received no treatment. Forty-eight hours later, scintigraphic imaging of the head and abdomen were performed with the radiolabeled P-glycoprotein substrate methoxy-isobutyl-isonitrile (sestamibi) in both groups of dogs. After a washout period of 60 days, the dogs in each group received the alternate treatment, and scintigraphic imaging again was performed 48 hours later. Gallbladder-to-liver and brain-to-neck musculature ratios of technetium Tc 99m sestamibi were calculated for each dog and compared between treatments.
Results—No significant differences in gallbladder-to-liver or brain-to-neck musculature ratios were found between treatments.
Conclusions and Clinical Relevance—Results provided evidence that spinosad did not inhibit P-glycoprotein function 48 hours after spinosad was administered at the manufacturer's recommended dose. Further investigations will be necessary to elucidate the mechanism of the reported toxic interaction between spinosad and ivermectin.
