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Effects of EDTA-induced Hypocalcaemia and Stress on Plasma TNF-alpha, IL-1-ra, G-CSF, GM-CSF and S-100 in Dairy Cows

Overview
Journal Vet Res Commun
Publisher Springer
Date 1999 Sep 24
PMID 10493117
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Abstract

The pathophysiology of postparturient paresis is still not completely understood. Knowledge recently acquired in immunology, endocrinology and cell physiology has still to be integrated in order to elucidate the aetiopathogenesis of the disease. For that purpose, the effect of the EDTA infusion model on the plasma concentrations of selected cytokines and growth factors, and of a calcium binding protein was examined in dairy cows. Six 6- to 11-year-old Brown Swiss cows in mid lactation were infused with a 5% solution of Na2EDTA in one jugular vein over a period of 5 h. Blood samples were collected from the contralateral side daily two days before, and then hourly for five hours during the infusion, hourly for five hours after the end of the infusion, and once daily for 10 days thereafter. The plasma concentrations of cortisol, tumour necrosis factor-alpha, interleukin-1 receptor antagonist, granulocyte colony-stimulating factor, granulocyte and macrophage colony-stimulating factor, and the calcium binding protein S-100 were determined. Before the EDTA infusion, during the infusion and for two days thereafter, the mean plasma concentrations of cortisol were significantly higher than those from days 4 to 10 after the infusion. The plasma concentrations of tumour necrosis factor-alpha and interleukin-1 receptor antagonist followed a similar profile. At the end of EDTA infusion, low concentrations of granulocyte colony-stimulating factor were detected in one cow only. On days 3 and 4, the mean plasma concentrations of granulocyte colony-stimulating factor were significantly higher than the pre-infusion values, but this was followed by a significant decrease on post-infusion day 5. From day 4 to 7, the plasma concentrations of S-100 were significantly lower than the pre-infusion values. The importance of these findings in the pathophysiology of postparturient paresis remains to be established.

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