Coagulation Tests and Selected Biochemical Analytes in Dairy Cows with Hepatic Lipidosis

The aim of this study was to determine the values and changes in conventional and optimised clotting tests, as well as in selected biochemical analytes during hepatic lipidosis in postpartum dairy cows. Ten healthy and ten Holstein cows with hepatic lipidosis were selected based upon clinical history, clinical examination, liver biopsy, flotation test and histological analysis of hepatic tissue. Prothrombin time (PT) and partial thromboplastin time (PTT) were determined in non-diluted and diluted blood plasma samples. Clotting times determined in diluted plasma samples were prolonged in cows with hepatic lipidosis and there was a difference in the PT value at both 50% and 25% plasma dilutions between both groups of animals (P = 0.004 and P = 0.001). Significant differences between healthy animals and cows with hepatic lipidosis were observed in blood serum values for free fatty acids (FFA), aspartate aminotransferase (AST) and triacyglycerols (P = 0.001, P = 0.007 and P = 0.044), respectively. FFA and liver biopsy are better diagnostic indicators for hepatic lipidosis than coagulation tests. The optimised PT is prolonged in cows with hepatic lipidosis and can detect this alteration that cannot be appreciated using conventional PT test

Upregulation of GH, but not IGF1, in the hippocampus of the lactating dam after kainic acid injury

Lactation embodies a natural model of morphological, neurochemical, and functional brain plasticity. In this reproductive stage, the hippocampus of the female is less sensitive to excitotoxins in contrast to nulliparity. Growth hormone (GH) and insulin-like growth factor 1 (IGF1) are known to be neuroprotective in several experimental models of brain lesion. Here, activation of the GH–IGF1 pituitary–brain axis following kainic acid (7.5 mg/kg i.p. KA) lesion was studied in lactating and nulliparous rats. Serum concentrations of GH and IGF1 were uncoupled in lactation. Compared to virgin rats, the basal concentration of GH increased up to 40% but IGF1 decreased 58% in dams, and only GH increased further after KA treatment. In the hippocampus, basal expression of GH mRNA was higher (2.8-fold) in lactating rats than in virgin rats. GH mRNA expression in lactating rats increased further after KA administration in the hippocampus and in the hypothalamus, in parallel to GH protein concentration in the hippocampus of KA-treated lactating rats (43% vs lactating control), as detected by Western blot and immunofluorescence. Except for the significantly lower mRNA concentration in the liver of lactating rats, IGF1 expression was not altered by the reproductive condition or by KA treatment in the hippocampus and hypothalamus. Present results indicate upregulation of GH expression in the hippocampus after an excitotoxic lesion, suggesting paracrine/autocrine actions of GH as a factor underlying neuroprotection in the brain of the lactating dam. Since no induction of IGF1 was detected, present data suggest a direct action of GH