The Role of Prostaglandins in Endometrial Vascular Changes at Implantation

Kennedy, T. G.; Armstrong, David T.

doi:10.1007/978-1-4613-3180-3_28

Cited by 36 publications

(18 citation statements)

References 53 publications

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“…One relevant factor in this context could be prostaglandins. Macrophages are known to secrete prostaglandins (Davies et ai, 1980) and prosta¬ glandins have been implicated in the control of implantation and decidualization (Kennedy & Armstrong, 1981). The observation that implantations of a second pregnancy do not occur in recently used zones of the uterus (rat: Momberg & Conaway, 1956;hamster: Orsini, 1962;bank vole: Nerquaye-Tetteh, 1986) cannot be accounted for by a failure to initiate decidualization at used sites, although the results reported here do suggest that recently used uterine areas are associ¬ ated with less decidual tissue than previously unused uterine areas.…”

Section: Resultsmentioning

confidence: 99%

Decidualization in the post-partum uterus of the mouse

Brandon

1990

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Summary. Unilaterally ovariectomized mice were allowed to complete one pregnancy before the second ovary was removed and sensitivity to decidualization was induced by hormone administration. The virgin uterine horn and the post-partum horn were stimulated to decidualize by the intraluminal injection of arachis oil. A greater decidual response was found in post-partum horns than in virgin horns. The foci of decidual induction in post-partum horns were regularly spaced reflecting the regular spacing of used and unused areas of the uterus. A focus of decidual induction occurred in 68% of the recently used uterine areas observed, i.e. areas associated with post-partum nodules. When compared with foci of decidualization in adjacent unused areas of the uterus, none of the decidualized used zones showed more decidual tissue, about half showed less decidual tissue and half showed the same amount of decidual tissue. The remaining 32% of used zones were not associated with foci of decidual induction. The results indicate that decidualization can be induced in recently used zones of the uterus using a non-traumatic method of induction, but that used zones are associated with less decidual tissue than unused zones of the post-partum uterus.

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Section: Resultsmentioning

confidence: 99%

Decidualization in the post-partum uterus of the mouse

Brandon

1990

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“…Since PGE-2 of uterine origin is apparently the main mediator in causing a local increase in capillary permeability at the site of implantation in the rat uterus (Kennedy & Armstrong, 1981), the reduced tissue concentration in and reduced output from the ageing rat uterus of PGE-2 may be one of the factors responsible for the lower implantation rate in older rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of age and steroid treatment on prostaglandin production by the rat uterus in relation to implantation

Brown¹,

Gosden²,

Poyser³

1984

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“…In all these species, the blastocysts undergo marked expansion prior to implantation. In contrast, attempts to demonstrate prostaglandin synthesis by rat (Kennedy and Armstrong 1981) or mouse (Racowsky and Biggers 1983) blastocysts, which remain small prior to implantation, have been unsuccessful, although the inhibition of hatching of mouse blastocysts in vitro by inhibitors of prostaglandin synthesis (Biggers et al 1978;Baskar et al 1981;Hurst and MacFarlane 1981) provides indirect evidence for its occurrence. However, demonstration of blastocyst prostaglandin production by itself is not sufficient; it is necessary to demonstrate that these prostaglandins act on the endometrium.…”

Section: Source Of Prostaglandinsmentioning

confidence: 99%

“…Arguing by analogy with the inflammatory response, Kennedy and Armstrong (1981) have suggested that there may be two mediators of the endometrial vascular permeability response; one, a prostaglandin of the E or I series, may cause vasodilation; the other, possibly histamine, may increase vascular permeability. In support of this are the observations that vasodilation accompanies the endometrial permeability response to an artificial stimulus (Bitton et al 1965) and, as reviewed above, that histamine may be involved in implantation.…”

Section: Mode Of Action Of Prostaglandinsmentioning

confidence: 99%

Embryonic signals and the initiation of blastocyst implanation.

Kennedy¹

1983

Aust. Jnl. Of Bio. Sci.

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The earliest sign of blastocyst implantation is an increase in endometrial vascular permeability which is localized in areas adjacent to blastocysts. The localized nature of this response suggests that it occurs in response to a signal from the blastocyst. It has been suggested that this signal may be physical in nature, or may be due to blastocyst-produced histamine, oestrogen or prostaglandins. The evidence for each of these is reviewed. At present, it is not possible to exclude any of these signals, which are not mutually exclusive, with certainty. The bulk of the evidence suggests that prostaglandins have an obligatory role in the initiation of implantation, but they may not necessarily be of blastocyst origin.

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The Role of Prostaglandins in Endometrial Vascular Changes at Implantation

Cited by 36 publications

References 53 publications

Decidualization in the post-partum uterus of the mouse

Decidualization in the post-partum uterus of the mouse

Effects of age and steroid treatment on prostaglandin production by the rat uterus in relation to implantation

Embryonic signals and the initiation of blastocyst implanation.

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