Background Development of equine platelet concentrate (PC) would aid management of cases requiring transfused platelets (PLTs), where adminstration of whole‐blood or platelet‐rich plasma (PRP) might be contraindicated. Objectives To test and validate a method for production of an equine PRP‐PC product. Animals Six healthy Thoroughbred geldings from a research herd. Methods In this prospective experimental study, whole blood was collected and processed through multiple centrifugation steps to yield 120 mL of PC. The PC was stored at 22°C and gently and continuously agitated. Measurements of PLT count, pH, and concentrations of glucose, lactate, electrolytes, lactate dehydrogenase (LDH), and aspartate aminotransferase (AST), as well as partial pressures of oxygen and carbon dioxide were performed on days 0, 1, 2, 3, 5, and 7. Platelet aggregometry and bacterial culture were also performed. Results The PC always had a PLT count of ≥550 × 10 3 cells/μL. Aggregometry graph amplitude ( P < .0001) and area under the curve ( P < .05) significantly decreased over time. Sodium, chloride, lactate ( P < .0001), and oxygen ( P < .01) concentrations significantly increased over time. pH ( P < .001), glucose and bicarbonate concentrations ( P < .0001) significantly decreased over time. There was no significant difference in potassium concentration, PLT count, LDH and AST activities and no bacterial growth from culture. Conclusions and Clinical Importance The described technique yielded a PC that meets the standards of the American Association of Blood Banks for human PC.

Two horses were referred for methemoglobinemia and hemolytic anemia following 5 acute deaths in their herd from an unidentified toxin source. Horses have a greater risk than other mammalian species of developing methemoglobinemia and hemolytic anemia following ingestion of oxidizing toxins, due to deficiencies in the mechanisms that protect against oxidative damage in erythrocytes. Their susceptibility to oxidative erythrocyte damage is evident in the numerous cases of red maple (Acer rubrum) toxicosis. The suspected toxins causing A. rubrum toxicosis are tannic acid, gallic acid, and a metabolite of gallic acid, pyrogallol. These compounds can be found in a variety of plants, posing a risk to equine health. In order to quickly identify toxin sources, 2 rapid in vitro assays were developed to screen plant extracts for the ability to induce methemoglobin formation or cause hemolysis in healthy equine donor erythrocytes. The plant extract screening focused on 3 species of the genus Pistacia: P. atlantica, P. terebinthus, and P. chinensis, which were located in the horse pasture. Extracts of the seeds and leaves of each species induced methemoglobin formation and resulted in hemolysis, with seed extracts having greater potency. The in vitro assays used in the current study provide a useful diagnostic method for the rapid identification of oxidizing agents from unidentified sources. There is no effective treatment for oxidative erythrocyte damage in horses, making rapid identification and removal of the source essential for the prevention of poisoning.

Platelet aggregometry results suggest that CPDA is superior to ACD for maintaining PLT viability following whole blood collection. This may be associated with the higher, more neutral pH as well as an increase in glucose available for metabolism. Although lactate was increased in the CPDA samples it was not high enough to decrease pH and therefore may not have been high enough to cause morphologic lesions and loss of PLT viability.

No abstract