Inflammation together with lipolysis and ketogenesis in early lactation can cause low productivity and may be harmful to the cow health. The objective of the study was to determine if ketoprofen treatment in the first days following parturition would positively affect the milk production and whether it was associated with the metabolic and inflammatory response. The study was conducted on 30 cows divided into two groups of 15 cows each. The experimental group was treated with 3 mg × kg. bw. -1 ketoprofen for three consecutive days after parturition. The blood samples were collected on the first day of treatment and in the first and second week postpartum and they were analyzed for non-esterified fatty acids (NEFA), beta-hydroxybutyrate (BHB), tumour necrosis factor-a(TNF-a) and haptoglobin. The results suggested that ketoprofen-treated cows with a higher milk production had a significantly lower concentration of NEFA, BHB, TNF-a and haptoglobin in the first and second week postpartum. No differences were found in the control group in metabolic status regardless of the achieved level of milk production. Ketoprofen administration in postpartum cows can enhance the milk yield. The higher milk yield in the experimental group might be associated with a lower degree of lipolysis, ketogenesis and reduced inflammatory response in the first two weeks postpartum.

Platelet aggregation contributes to the pathogenesis of cardiovascular diseases. After activation it leads to dense granule secretion and 5-HT release. The question arises; how platelet aggregation is endogenously controlled during blood circulation. In preliminary studies, we observed that human plate-lets aggregate more rapidly when suspended in buffer as compared to those suspended in plasma (PRP). These observations point to the presence of an endogenous substance that may inhibit arachidonic acid– induced platelet aggregation. An analysis of plasma Cohn fractions demonstrated that most of the plasma inhibitory activity was associated with albumin–rich and α-globulin rich protein fractions. The identity of plasma endogenous inhibitors of platelet aggregation (EIPA) was established by affinity chromatography on Cibacron Blue F3G-A for specific removal of albumin. The association of α-globulins to EIPA activity was recognized as due to haptoglobin by affinity chromatography on a column of hemoglobin-sepharose. In addition, we also found that the distribution of EIPA activity varies according to sex and physiological state. These findings reveal that EIPA may act by modulation of arachidonic acid metabolism or seques-tering the fatty acid substrate.