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Biomedical subjects

R Magness

Publications and source records attributed to R Magness.

5 recordsLinked to original sources

Inhibition of an IUD-induced precocious luteolysis by prostaglandin E1 (PGE1) in sheep.

Fifteen ewes were assigned as they came into estrus to one of three randomized treatment groups: 1. Sham IUD + Vehicle, 2. IUD + Vehicle or 3. IUD + PGE1 in vehicle. An IUD was inserted adjacent to the luteal-bearing ovary on day 3 postestrus. Prostaglandin E1 (500 micrograms) in vehicle (Na2CO3) or vehicle was given intrauterine through an indwelling uterine cannula every four hours from day 3 postestrus until ewes returned to estrus. Precocious estrus was induced in both the sham IUD and IUD groups receiving vehicle. Prostaglandin E1 prevented an IUD-induced premature luteolysis based on daily concentrations of progesterone in peripheral blood and the interestrous interval. It is concluded that an IUD-induced premature luteolysis is not necessarily via physical distention by the IUD. It is also concluded that chronic intrauterine infusions of PGE1 can prevent an IUD-induced premature luteolysis.

Alprostadil↗

Effects of prostaglandin E2 (PGE2) on estradiol-17 beta-induced luteolysis in the nonpregnant ewe.

Fifteen ewes were assigned as they came into estrus to the following randomized treatment groups: 1) Vehicle (1 ml corn oil + vehicle Na2CO3 buffer), 2) Estradiol-17 beta + vehicle and 3) Estradiol-17 beta + PGE2 (500 micrograms) in Na2CO3 buffer (5 ewes/treatment group). Prostaglandin E2 was given through an intrauterine cannula every four hours from days 8 through 15 postestrus. PGE2 prevented a luteolytic dose of estradiol-17 beta given on days 9 and 10 from causing a precocious luteolysis. PGE2 maintained concentrations of progesterone in peripheral blood (days 8 through 15) and weights and concentrations of progesterone in corpora lutea on day 15 postestrus of ewes receiving estradiol-17 beta. It is concluded that chronic intrauterine infusions of PGE2 can prevent an estradiol-17 beta-induced premature luteolysis.

Animals↗

Effects of prostaglandin E1 (PGE1) on estradiol-17 beta induced luteolysis in the nonpregnant ewe.

Nonpregnant ewes were assigned as they came into estrus to one of the following randomized treatment groups: 1) Vehicle (1 ml corn oil) + Vehicle (buffer), 2) Estradiol-17 beta + Vehicle (buffer) or Estradiol-17 beta + PGE1 in buffer. Ewes were unilaterally ovariectomized on day 8 postestrus and an intrauterine cannula was installed in the uterine horn adjacent to the remaining luteal-bearing ovary. Buffer of PGE 1 (500 micrograms) in buffer was infused intrauterine every 4 hours from day 8 through day 15. Luteolysis was initiated by giving an intramuscular injection of estradiol-17 beta (500 micrograms) on days 9 and 10. Chronic intrauterine infusions of PGE1 maintained jugular progesterone through day 15 and weights of corpora lutea and progesterone in corpora lutea on day 15 although luteolysis was initiated by estradiol. It is concluded that chronic intrauterine infusions of PGE1 can prevent an estrogen-induced premature luteolysis.

Alprostadil↗

Prostaglandin E2 (PGE2) inhibits an IUD-induced premature luteolysis in sheep.

Fifteen ewes were assigned as they came into estrus to one of three randomized treatment groups: 1. Sham IUD + Vehicle, 2. IUD + Vehicle, and 3. IUD + PGE2 in Vehicle. An IUD was inserted adjacent to the luteal-bearing ovary of unilaterally ovariectomized ewes on day 3 postestrus. Vehicle (Na2CO3) or PGE2 (500 micrograms) in vehicle was given every 4 hours intrauterine through an indwelling uterine cannula from day 3 postestrus until ewes returned to estrus. Luteolysis was advanced in both the Sham IUD and IUD groups receiving vehicle. An IUD-induced premature luteolysis was prevented by PGE based on daily concentrations of progesterone in peripheral blood and the extended interestrous interval. It is concluded that chronic intrauterine injections of PGE2 (500 micrograms) every four hours can prevent an IUD-induced premature luteolysis. It is also concluded that an IUD-induced premature luteolysis is not necessarily through uterine distention.

Animals↗

Development of the rabbit visual cortex: a quantitative Golgi analysis.

Lamina IV stellate cells and lamina V pyramidal cells were studied in Golgi material of visual cortex of rabbits ranging in age from 10 days to adult. Spine density counts revealed that primary branches have lower spine density than secondary or tertiary branches in both stellate and basilar pyramidal dendrites. Most areas sampled showed an increase in spine density from age 10 days to a peak at 25-30 days. In some areas this was followed by a plateau, but in most dendritic areas sampled there was a significant decrease from peak levels to adult levels. Measurements of dendritic length revealed that basilar dendrites undergo changes in length which parallel the changes in spine density counts: a peak in the length of basilar dendrites was followed by a decline to adult levels. However, the dendritic length of stellate cells showed much less change with age after 10 days. We propose that the time period during which spine density and pyramidal cell dendritic organization peaks above adult levels may coincide with, and provide a morphological correlate of, the critical period.

Aging↗