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This study analysed the relaxant properties of salbutamol (β₂₋adrenoceptors agonist) and BRL 37344 (β₃₋adrenoceptors agonist) regarding the contractility of porcine myometrium on days 10-14 of the oestrous cycle (cyclic group; n = 10) and on days 3-5 of pregnancy (early pregnant group; n = 6). The activity of myometrial strips (tension, frequency and amplitude) was recorded under isometric conditions using force transducers. The contractility was assessed further following the administration of increasing concentrations of the agonists (10⁻⁹-10⁻⁴ M), both with and without β-adrenoceptor antagonists (butaxamine – a selective β₂₋ adrenoceptor antagonist, propranolol- a non-selective β₁₋and β₂₋adrenoceptor antagonist and bupranolol – a non-selective β₁₋, β₂₋ and β₃₋adrenoceptor antagonist) at a concentration of 10⁻⁴ M. Although neither salbutamol nor BRL 37344 caused changes in the tension, at the highest concentrations they decreased the frequency and amplitude of contractions. These changes were more evident after salbutamol treatment and in the early pregnant group. Antagonists given alone did not cause changes in the parameters examined but changed some activity of the agonists. Butoxamine reduced the decrease in frequency and amplitude induced by salbutamol and produced a decrease in the tension after BRL 37344 treatment in the early pregnant group. Propranolol reduced the decrease in frequency and amplitude induced by salbutamol in both examined groups and did not cause significant changes in BRL 37344 activity. The administration of bupranolol before salbutamol treatment caused an increase in the tension and reduced the decrease in the frequency in the cyclic group. Moreover, bupranolol eliminated a decrease in frequency and induced an increase in amplitude caused by BRL 37344 in both groups and these changes were more evident in the early pregnant group. The data indicates that both β₂₋ and β₃₋adenoreceptors are involved in the regulation of the contractility in both groups, but the changes after agonists and antagonists treatment are more evident in the early pregnant myometrium.
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Toxicity of salinomycin and narasin in turkeys

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Coccidiosis continues to be one of the most serious diseases in poultry breeding, causing major economic losses in this industry. Many trials are conducted to prevent and control this disease. However, only a few medications are approved for use in the prevention and treatment of coccidiosis. Ionophore coccidiostats (e.g. salinomycin and narasin) act by altering the transmembrane movement of monovalent or divalent ions (Na+, K+, Ca2+, Mg2+, Rb+, Cs+), resulting in altered ionic gradients and disturbed physiological processes in coccidia. In broiler and turkey breeding, these agents are used for nearly the whole fattening period. Ionophore coccidiostats have a narrow safety margin. Their toxicity is probably due to a disturbed ion balance or to oxidative damage. Although ionophore coccidiostats are considered to be relatively safe for target animals, there are numerous reports of poisoning cases caused by these medications in birds. This paper summarizes the current state of knowledge on the toxicity of salinomycin and narasin in turkeys. It reviews the data concerning the symptoms, mortality rate and possible causes of poisoning with these agents. Moreover, the paper discusses the legal regulations regarding the use of these drugs in poultry.
Non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely used drugs in both human and veterinary medicine. NSAIDs inhibit the enzyme cyclooxygenase in the arachidonic acid cascade. This mechanism results in a reduced or blocked synthesis of prostaglandins. Eicosanoids are very important for reproduction and their inhibition by NSAIDs may cause disorders in the ovarian cycle. The article summarizes the latest knowledge about the effects of NSAIDs on corpus luteum function.
The aim of the study was to determine whether treatment with recommended doses of meloxicam or flunixin had an effect on the apoptosis of peripheral blood T lymphocytes in calves. The study was carried out on 4-5 months old calves (n = 24, 8 per group). Experimental animals were injected subcutaneously with a single dose of 0.5 mg . kg-1 of meloxicam or intravenously with 3 doses of 2.2 mg . kg-1 day-1 of flunixin. The non-treatment animals served as control. Blood samples were taken at day 0 and at days 1, 2, 3, 5, 7 and 14 after the first NSAIDs injection. Apoptosis was determined by flow cytometry using Annexin V-PE/7-AAD staining. The kinetic analysis of apoptosis in the total lymphocyte population, as well as in the CD4+ and CD8+ subsets did not reveal significant differences in the frequency of early apoptotic cells between control and experimental groups throughout the period studied. Although, 24 h after administration of the first dose of NSAIDs, late-stage apoptosis/necrosis was significantly increased in the total lymphocyte population (the meloxicam group), as well as in the CD4+ (the meloxicam group and the flunixin group) and CD8+ (the flunixin group) subsets of T cells. However, this disturbance was transient, relatively poorly expressed and, thus, unlikely to be of clinical significance. Our results indicate that the use of meloxicam or flunixin in accordance with the recommended dosage regimen in cattle do not have a clinically significant influence on apoptosis of peripheral blood T cells.
The objective of the present study was to determine the influence of nonsteroidal anti-inflammatory drugs (NSAIDs) representing different chemical groups on progesterone (P₄) production by cultured bovine steroidogenic luteal cells. The cells were enzymatically isolated from corpora lutea collected on days 8-12 of the estrous cycle. After 24 h preincubation they were incubated for 24 h with medium only (control) or stimulated with bovine luteinizing hormone – LH (100 ng/ml; positive control) or increasing concentrations (10⁻⁸ to 10⁻⁴ M) of acetylsalicylic acid, indomethacin, ibuprofen, naproxen, piroxicam, phenylbutazone, dipyrone or nimesulide. Concentartions of P₄ in the culture media were determined by enzyme immunoassay. LH significantly increased P₄ secretion, while acetylsalicylic acid and indomethacin did not affect the production of this hormone. A significant increase in P₄ secretion was observed after administration of dipyrone at all concentrations, piroxicam at concentrations of 10⁻⁸, 10⁻⁷ and 10⁻⁵ M, phenylbutazone and naproxen at concentrations of 10⁻⁷ and 10⁻⁶ M and ibuprofen at concentrations of 10⁻⁵ and 10⁻⁴ M. Nimesulide did not affect P₄ production at concentrations of 10⁻⁸ – 10⁻⁵ M, while at a concentration of 10⁻⁴ M it inhibited P₄ secretion. The results obtained indicate that NSAIDs may change the production of P₄ in bovine luteal cells, however, these changes are dependent on the substance used.
A chemically synthesized gene coding for the serine proteinase inhibitor CPTI II was cloned in E. coli and its expression was investigated in cytoplasmic and secretion systems. Under all conditions investigated the biologically active form of the inhibitor was found only in the latter system, although the yield was rather low.
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