The effects of a number of non-steroidal anti-inflammatory compounds on parturition in the rat

Powell, J. G.; Cochrane, Robert L.

doi:10.1016/0090-6980(82)90110-1

Cited by 15 publications

(2 citation statements)

References 33 publications

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“…Perraud et al [1984] demonstrated a lack of embryotoxicity and teratogenicity in rats and rabbits treated with piroxicam in doses of 2-10 mg/kg. Such results were partially confirmed by others [Sakai et al, 1980;Powell and Czochrane et al, 1982]. The prenatal DFU data are similar to those reported for other selective COX-2 inhibitors, including DuP-697 ], celecoxib and rofecoxib [PDR, 2003].…”

Section: Discussionsupporting

confidence: 80%

Cyclooxygenase Inhibitors Affect Bone Mineralization in Rat Fetuses

Burdan

Różyło‐Kalinowska²,

Szumiło³

et al. 2007

Cells Tissues Organs

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Intrauterine growth retardation, increased incidence of developmental variations, lack of cartilage and joint developmental side effects were previously reported for nonselective (ibuprofen, piroxicam, tolmetin) and selective (DFU) cyclooxygenase (COX)-2 inhibitors, also known as nonsteroidal anti-inflammatory drugs. The aim of the present study was to evaluate the lumbar vertebra mineralization in fetuses prenatally exposed to COX inhibitors. All the tested compounds were administered intragastrically to pregnant rats from gestational days 8 to 21. Fetuses were delivered on gestational day 21, and after digital radiological examination were double-stained with alcian blue and alizarin. Decrease of alizarin staining, as a qualitative sign of mineralization, was significantly greater in groups exposed to the highest doses of the nonselective COX inhibitors. Decrease of vertebra mineralization in drug-exposed groups was also revealed using quantitative radiological analysis. However, significant differences were noted only for the fifth and sixth lumbar vertebrae in the group exposed to the highest dose of tolmetin. Strong influence of the total protein level in maternal sera on the fetal bone optic density was found. It should be stressed that unlike DFU, the examined nonselective COX inhibitors decreased fetal bone mineralization when administered in high maternal toxic doses. Moreover, maternal health status determined fetal bone mineralization.

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Section: Discussionsupporting

confidence: 80%

Cyclooxygenase Inhibitors Affect Bone Mineralization in Rat Fetuses

Burdan

Różyło‐Kalinowska²,

Szumiło³

et al. 2007

Cells Tissues Organs

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“…The objective of this experiment was to determine whether the PGF2, signal could be blocked during a pine needle-induced parturition. This was tested by feeding a prostaglandin inhibitor (ketoprofen, Kubota et al, 1979;Powell and Cochrane, 1982;Ueno et al, 1987) during the time of pine needle feeding. Fifteen cows were assigned to one of three treatments (Table 4).…”

Section: Experiments 3 Progesterone Decreases Dramaticallymentioning

confidence: 99%

Endocrine responses in cows fed Ponderosa pine needles and the effects of stress, corpus luteum regression, progestin, and ketoprofen.

Short

Staigmiller²,

Bellows³

et al. 1995

Journal of Animal Science

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Pregnant cows were fed pine needles (PN, 2 kg.cow-1.d-1) mixed with the diet to determine factors that affect abortion response. In Exp. 1, treatments were used to determine the effects of experimental stress and pelleting of pine needles. Pelleting needles and experimental stress delayed abortion response (P < .01). Stress-induced delay was associated with abnormal patterns of progesterone and cortisol (P < .01). In Exp. 2A and 2B, the role of the corpus luteum (CL) in abortion response to PN consumption was investigated by regressing the CL with prostaglandin F2 alpha. Regression of the CL and PN feeding reduced interval to parturition, but the effect of PN feeding was less when the CL was regressed (PN x CL, P < .01). The progesterone increase in response to experimental stress was decreased by CL regression (P < .01). In Exp. 3, melengestrol acetate (MGA) was fed (0, 2, or 4 mg.cow-1.d-1) in addition to PN. Parturition was blocked more effectively as dose of MGA increased (P = .075), but only parturition was blocked rather than the effects of PN. In Exp. 4, CL regression was blocked by feeding ketoprofen. Ketoprofen delayed response to PN, but the effect was only temporary (P < .01). Our conclusions are that 1) experimental stress delays abortion response to PN by increased concentrations of progesterone, 2) pelleting PN decreases their abortifacient activity, and 3) abortions caused by PN can be blocked by feeding a progestin or a prostaglandin inhibitor, but these compounds do not block the primary abortifacient effects of PN.

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