During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and kidney ADRs in the fetus. Additionally, they are linked with premature birth and miscarriage. Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies. Additionally, indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal kidney blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy, but Leffers et al. released a study in 2010 indicating that there may be associated male infertility in the unborn. Doses should be taken as prescribed, due to risk of liver toxicity with overdoses.

In France, the country's health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy

Reproductive system

Prostaglandins have extensive involvement in the reproductive system. They are associated with ovulation,

oviposition, and luteal function. In reptiles, prostaglandins have been shown to stimulate oviducal contractions,

which may be overridden by neural control, which can subsequently result in egg retention.

Jones et al dem-

onstrated that a prostaglandin inhibitor (indomethacin) delayed FSH-induced ovulations, lowered PGE secre-

tion, and inhibited preovulatory changes in the follicular wall in anoles.

Mahmoud et al showed that a single

injection of PGF

2α

in recently ovulated snapping turtles induced early luteolysis and a significant decrease in

plasma progesterone levels.

Late pregnancy in common geckos, a viviparous species, could not be induced

to give birth with high doses of PGF

2α

unless the animal was pretreated with a β-adrenergic antagonist in vivo,

whereas in vitro, administration of PGF

2α

caused uterine contraction, which could be blocked by administration

of a β-adrenergic agonist.

In 1992, Gobbetti et al showed that in the brains of crested newts, PGF

2α

is involved

in the post-reproduction processes through estradiol secretion, while PGE

2

was involved in the reproductive

processes, possibly through androgen secretion.

In 1994, Gobbetti et al studied prostaglandins in the brains of

Italian wall lizards during reproduction and found that PGF

2α

levels were elevated during the refractory phase

of the reproductive cycle, whereas PGE

2

levels were decreased. They also determined that levels of PGF

2α

were

increased after treatment with salmon GnRH, and decreased by substance P and acetylsalicylic acid.

Dubois

and Guillette demonstrated that the uteri of alligators secrete PGE and PGF

2α

at varying levels depending on the

reproductive status of the animal.

In 1994, Gobbetti et al looked at prostaglandins in the reproductive cycle

of male Italian wall lizards, and found that testicular androgen synthesis during the fighting phase is under the

control of PGE

2

, whereas 17β-estradiol synthesis during the refractory phase is regulated by PGF

2α

in the testes,

and by PGE

2

and PGF

2α

in interrenal cells.

In 2006, Jones et al looked at the interactions between uterine ten-

sion, PGs, calcium and AVT in the uteri of anoles, and noted that indomethacin blocked the AVT-induced tonic

contractions in stretched uteri, and that the interval between contractions was decreased by PGF

2α

and PGE

2

,

an effect that was also blocked by indomethacin.

In amphibians, Guillette et al noted that ovarian and oviducal PGF

2α

acts like an endocrine hormone, coordinat

-

ing oviducal contractions and CNS-controlled oviposition behavior.

Diakow and Nemiroff showed that PGE

2

and PGF

2α

affect female mating behavior in leopard frogs, and that vasotocin acts in part through a mechanism

that involves prostaglandin synthesis.

In 1992, Gobbetti and Zerani showed that testicular PGF

2α

was lower

in the post-reproduction phase in edible frogs, and that administration of mammalian GnRH increased its levels

during the pre-reproduction and reproduction phases.

In crested newts, testicular PGF

2α

levels were lower

during the reproduction phase, and administration of GnRH increased its levels during the pre-reproduction

and reproduction phases.

They also showed that PGF

2α

levels were increased in ovulating edible frogs, and it

may be involved in the control of egg deposition in this species.

In 1993, Gobbetti and Zerani showed that in

edible frogs, a seasonal increase in plasma PGE

2

may inhibit breeding activity by stimulating ovarian androgen

secretion, whereas a seasonal increase in plasma PGF

2α

may inhibit breeding by stimulating ovarian estradiol

secretion.

In 1995, Chang et al demonstrated that elevated levels of PGF

2α

are associated with spontaneous

hormone-induced ovulation, and that protein kinase C mediates gonadotropin induction of PGF

2α

in the ovaries

of

Rana sp

In leopard frogs, Schuetz noted that normal synchronization and maturation of oocytes may require

the combined action of steroids and prostaglandins acting within different follicular compartments.

Ramos et

al found that PGF

2α

increased ovulation induced by a pituitary homogenate in toad ovaries, whereas PGE

1

had

an inhibitory effect on ovulation.

thank you for your answers, andI have all the respect and appreciation for you

All the informations were useful .

But I need to know if there is any effect of dipyrone on first half of pregnancy in rats

Karyometric results showed that the nuclear volumes of placental cells in rats treated with dipyrone during the first 3 periods were significantly greater than in control animals and that, closer to term, no differences were observed in this regard. Only the animals treated from the 9th to the 12th day of pregnancy had higher placental contents of DNA, RNA and protein than the corresponding controls. results showed that dipyrone had a blocking effect on placental cell division which occurs mainly in the initial steps of placental development.

increased risk for malformations or perinatal complications, including preterm birth or low birth weight