Prostaglandin Content Research Articles

EFFECT OF GONADOTROPIN AND ESTROGEN ON CHANGES IN LEVELS OF PROSTAGLANDIN IN RAT OVARY

AbstractEffects of gonadotropin and estrogen on the levels of prostaglandin (PG) in the rat ovary were investigated. PGF content in rat ovary, as measured by radioimmunoassay, was slightly higher than that by bioassay using rat stomach fundus, although there was no statistically significant difference. PGE and PGF levels in rat ovary during the estrous cycle were lowest on the day of diestrus, PGE was of the highest level on the day of estrus, and PGF on the day of proestrus. Both PGE and PGF were increased 24 hours after treatment with pregnant mare serum gonadotropin on the first day of diestrus. PGE was increased about 2.5 fold and PGF about 2.3 fold. PGF was significantly increased 24 hours after treament with estradiol on the first day of diestrus. These results suggest that gonadotropin may directly or indirectly regulate changes in ovarian PG content via actions of estrogen.

Effect of gonadotropin and estrogen on changes in levels of prostaglandin in rat ovary.

Effects of gonadotropin and estrogen on the levels of prostaglandin (PG) in the rat ovary wer investigated. PGF content in rat ovary, as measured by radioimmunoassay, was slightly higher than that by bioassay using rat stomach fundus, although there was no statistically significant difference. PGE and PGF levels in rat ovary during the estrous cycle were lowest on the day of diestrus, PGE was of the highest level on the day of estrus, and PGF on the day of proestrus. Both PGE and PGF were increased 24 hours after treatment with pregnant mare serum gonadotropin on the first day of diestrus. PGE was increased about 2.5 fold and PGF about 2.3 fold. PGF was significantly increased 24 hours after treatment with estradiol on the first day of diestrus. These results suggest that gonadotropin may directly or indirectly regulate changes in ovarian PG content via actions of estrogen.

15-hydroxyprostaglandin dehydrogenase and Δ 13 reductase content of gastrointestinal organs of rabbits and rats

15-Hydroxyprostaglandin dehydrogenase was measured in various gastrointestinal and non-gastrointestinal tissues from rabbits and rats. In addition, Δ 13 reductase activity was measured in fundic and antral mucosae and gastric muscle from rabbits. In rabbits, antral mucosa contained the greatest activity of 15-hydroxyprostaglandin dehydrogenae and was 6 times more active than rabbit lung and fundic mucosa. In rat, duodenal mucosa was more active than antral mucosa or pancreas, suggesting that interspecies variations may exist. Δ 13 reductase in rabbit gastric tissues was also more active in antral mucosa than in fundic mucosa or gastric muscle. The high activities of these enzymes in antral mucosa in conjunction with the known large prostaglandin content, particularly PGE 2 and PGI 2, suggest a large biological turnover of prostaglandin in these tissues.

Uterine catecholamines and prostaglandins during the estrous cycle of the rat.

The uterine contents of norepinephrine, epinephrine, dopamine, and prostaglandins F and E were determined on each day of the rat estrous cycle. Catecholamines were determined by high performance liquid chromatography with electrochemical detection (HPLC-EC) as well as by a radioenzymatic technique; prostaglandins were quantitated by RIA. The norepinephrine and dopamine values obtained by the radioenzymatic assay were approximately 1.5 times as high as the values obtained by HPLC-EC (norepinephrine, 285 vs. 188 ng/g; dopamine, 11.0 vs. 7.5 ng/g). Despite this difference in levels, both analytic techniques showed a decline in uterine norepinephrine from diestrus to estrus, followed by a significant (P less than 0.01) increase in norepinephrine on the day of metestrus. A cyclic pattern was also revealed for uterine dopamine concentration. There was a decline in dopamine concentration from diestrus to proestrus (radioenzymatic, P less than 0.01), followed by a return to high levels at metestrus (HPLC-EC). Epinephrine levels were low (undetectable by radioenzymatic assay; 24 ng/g by HPLC-EC) and showed no variation during the estrous cycle. Prostaglandin F was uniformly higher than prostaglandin E (10 vs. 2.5 ng/uterus). Significant increases in the uterine contents of both prostaglandins were shown on the day of proestrus.

Lymphocyte Cyclic Nucleotide and Prostaglandin Content in Psoriasis: A Preliminary Report

Lymphocytes from psoriatic patients were found to contain reduced levels of adenosine 3':5'-cyclic phosphate, guanosine 5'-cyclic phosphoric acid, and prostaglandin E, as compared with lymphocytes from normal subjects. The difference in prostaglandin F levels between psoriatic and control subjects was not statistically significant. These results could point to an immunologic defect in the immune system in psoriasis.

Lymphocyte cyclic nucleotide and prostaglandin content in psoriasis: a preliminary report

Lymphocyte cyclic nucleotide and prostaglandin content in psoriasis: a preliminary report

The role of eosinophils in granulopoiesis. I. Eosinophilia in neutropenic pateints

The role of eosinophils in granulopoiesis is unclear. In a variety of conditions, the level of eosinophils is inversely related to the level of neutrophils. The present report describes two patients with eosinophilia and neutropenia and examines the in vitro effects of eosinophils on the colony formation of their bone marrow in semisolid culture medium. The addition of autologous eosinophils to bone marrow cultures from these patients resulted in a decrease in the number of colonies; in contrast, antieosinophilic serum increased the number of colony-forming units. Indomethacin, an inhibitor of prostaglandin, was capable of reversing the effects of added eosinophils. The findings suggest that eosinophils have an inhibitory effect on in vitro granulopoiesis. The suppressive effects may be due to the high content of prostaglandin E found in eosinophils. A schematic diagram based on the current knowledge of the mechanism of granulopoiesis is presented.

Renal concentrating defect in the hypokalemic rat is prostaglandin independent.

The renal concentrating defect in the hypokalemic rat is prostaglandin independent. The present study was undertaken to test whether the renal concentrating defect in potassium-depleted rats is at least in part mediated by prostaglandins. Rats on a K-deficient (n = 12) and K-supplemented (n = 12) diet underwent a urinary concentrating test before and after prostaglandin inhibition with indomethacin. The drug did not alter maximal urinary osmolality in normokalemic rats. Likewise, the abnormal maximal urinary osmolality of K-depleted rats was not improved by prostaglandin inhibition (1,533 +/- 124 before and 1,475 +/- 88 mosmol/kg H2O after indomethacin). Control animals receiving a blank diluent instead of indomethacin showed no change in maximal concentrating ability between equally timed dehydration tests. Indomethacin caused no significant alterations in blood urea nitrogen or creatinine. Direct measurements of renal medullary prostaglandings revealed no difference between K-depleted (22.9 +/- 4.4 pg/mg) and normokalemic (23.6 +/- 2.3 pg/mg) rats. Indomethacin significantly and comparably lowered prostaglandin content in both K-depleted and normokalemic rats. These studies, therefore, reveal no enhancement of prostaglandin synthesis with K depletion and demonstrate that the renal concentrating defect of K depletion in the rats is prostaglandin independent.

Prostaglandins in the salivary glands and reproductive organs of Hyalomma anatolicum excavatum Koch (Acari: Ixodidae)

AbstractProstaglandin F (PGF) and E2 (PGE2) were assayed in the reproductive organs, salivary glands and egg-batches of laboratory-bred males and females of Hyalomma anatolicum excavatum Koch. Salivary glands and reproductive organs were dissected from unfed male and female ticks as well as from ticks that had fed for six days on rabbits; these organs were cultured for 24 and 72 h in tissue culture medium-199 with Earle's salt and HEPES buffer at pH 7·6 and 37°C. The amounts of PGF and PGE2 accumulated in the culture were determined by a radioimmunoassay using specific antibodies. Both salivary glands and reproductive organs were shown to synthesise PGEa and PGF. This synthesis and also the prostaglandin content of the organs were significantly increased after engorgement. The synthesising capacity and content of PGE2 and PGF in both the salivary glands and reproductive organs were higher in the female than in the male.

Heart adaptation to acute pressure overload: an involvement of endogenous prostaglandins.

The purpose of this investigation was to study the relationships between the contractile behavior of the heart and myocardial prostaglandins. Using an open-chest model in rabbits, we assayed the left ventricular tissue content to prostaglandins (PG) E and F2 alpha at various intervals following acute pressure overload created by graduated aortic stenosis. The results suggest that the rabbits could be divided into two distinct groups based on specific hemodynamic changes following coarctation (systolic and diastolic pressure, dP/dt, and contractility index). The first group included rabbits whose adaptation to pressure overload was expressed as a gradual increase in the contractility index. The second group was comprised of rabbits that developed heart failure following coarctation. The increase in contractility in response to overload in the first group was paralleled by an increase in the content of PGE and PGF 2 alpha in the left ventricle, whereas, in rabbits with heart failure, the prostaglandin level did not rise above that of the control hearts. It is suggested that an increased endogenous prostaglandin content may be an important factor in adaptation to acute overload.

The production of prostaglandins in response to experimentally induced osteomyelitis in rabbits

Osteomyelitis was induced in the tibiae of rabbits by injection of staphylococcus aureus and sodium tetradecylsulphate (STD); additional rabbits were injected with STD alone. Confirmation of osteomyelitis was based on positive culture of the same phage type bacteria from the tibiae and on the characteristic radiographical and histological appearance of osteomyelitis. Only tibiae which proved to be infected by the above criteria showed significantly increased in vitro release and content of Prostaglandin E and Prostaglandin F 2∝ compared with tibiae injected with STD (P < 0.05). After two weeks infection, infected tibiae released nine times more Prostaglandin E and five times more Prostaglandin F 2∝ than tibiae injected with STD alone.After four weeks infection,infecied tibiae released less Prostaglandin E (P< 0.05)than after two weeks infection but the release of Prostaglandin F 2σ was similar. The production of large amounts of prostaglandins by bones in response to infection may be the cause of the rapid bone resorption and sequester formation observed in osteomyelitis.

19-Hydroxy-prostaglandin e and infertility in human males

We measured the content of 19-hydroxy-prostaglandin E (19-OH-PGE) and prostaglandin E (PGE) in the semen of 10 infertile males by alkaline dehydration, thin layer chromatographic separation and ultraviolet spectrophotometry. 7 fertile males were also studied. In both groups the content of seminal 6-keto prostaglandin F lα (6-keto-PGF 1α) also was measured by thin layer chromatographic separation and highly specific radioimmunoassay. The amounts of 19-OH-PGE and PGE were significantly lower (p<.02, p<.05) in the infertile group than the fertile group. Differences in mean seminal 6-keto-F 1α were not significant. The uterine stimulatory actions of 19-OH-PGE demonstrable in the monkey may apply to fertility in man.

Prostaglandins and the sources of their production in a mild inflammatory lesion in sheep.

1. Wound fluid was collected from a subcutaneous lesion in the shoulder region of sheep by implanting a PTFE sampling chamber from which a catheter led to the skin surface. 2. The neutrophil granulocyte numbers and prostaglandin content of the wound fluid were studied, prostaglandins being identified by thin layer chromatography and measured by bio-assay. The major prostaglandin component was E2. 3. There was no clear relation between the amounts of prostaglandin present and the numbers of neutrophils in the fluid. 4. A subcutaneously implanted double chamber permitted perfusion of the lesion and thereby the study of the rate of prostaglandin production and the rate of disappearance of isotopically labelled prostaglandin from the lesion. The rate of leucocyte entry into the wound fluid could also be measured. 5. When the cutaneous muscle through which the chamber had been implanted was biopsied and incubated in vitro it was found to produce prostaglandin E2 in quantities which could be correlated with the weight of the incubated muscle. 6. These results suggest that a major contributor to the prostaglandin content of the wound fluid is the cutaneous striped muscle.

INVOLVEMENT OF PROSTAGLANDINS IN THE INHIBITION OF GROWTH HORMONE PRODUCTION IN CULTURED PITUITARY CELLS BY INSULIN

The effect of insulin was tested on the rate of synthesis and release of growth hormone in cultured rat anterior pituitary cells. Concentrations of insulin between 10(-9) and 10(-7) mol/l (6--600 ng/ml or 0.15--15 mu./ml) inhibited synthesis of growth hormone; 10(-8) mol insulin/l was most effective. The effect was observed after a time-lag of at least 1 h. Insulin at concentrations between 3 x 10(-9) mol/l and 3 x 10(-7) mol/l also inhibited growth hormone secretion in 30 min incubations. The most effective insulin concentration in this case was 3 x 10(-8) mol/l. Insulin (10(-9)-10(-7) mol/l) also decreased the intracellular content of prostaglandins E and F. The effect was rapid, reaching a maximum after 30 min. Indomethacin, an inhibitor of prostaglandin synthetase, dramatically lowered the concentration of prostaglandins in the cells within 30 min; growth hormone synthesis was also decreased, but not until after 2 h of incubation. The results suggest that an initial response to insulin treatment is a lowering of intracellular levels of prostaglandins, which may then mediate a decrease in growth hormone synthesis, after a 1--2 h delay.

The effect of essential fatty acid‐deficient diet on the levels of prostaglandins and their fatty acid precursors in the rabbit brain

AbstractRabbits were maintained on an EFA‐deficient diet. After eight weeks on this diet, lipid analysis showed no major alterations in the levels of brain dihomo‐gamma‐linolenic and arachidonic acids when compared with animals maintained on the standard laboratory diet. However, there were substantial reductions in the brain prostaglandin contents. It is suggested that the dihomo‐gamma‐linolenic acid and arachidonic acid utilized for prostaglandin production may be more directly related to the dietary essential fatty acid input rather than to the size of the precursor pool in the principal phospholipids.

Changes in intracellular prostaglandin content during activation of lymphocytes by phytohaemagglutinin

Changes in intracellular prostaglandin content during activation of lymphocytes by phytohaemagglutinin

Increased blood level of prostaglandin-like substances during cardiopulmonary bypass in the dog

Total heart-lung bypass (TBP) for open-heart surgery is often accompanied by a progressive reduction of systemic blood pressure. Since the lung is the main site of elimination of prostaglandins (PGs) from venous blood, TBP may lead to an increase in blood content of vasodilator PGs. TBP was performed in dogs and blood level of prostaglandinlike substances (PLS) was monitored continuously by a bio-assay method. The concentration of PLS increased during TBP to 0.8 ng.cm(-3) blood (in PGE2 equivalents). Restoration of normal circulation led to the disappearance of PLS from the blood. The increase in PLS during TBP was abolished by indomethacin. This was invariably accompanied by elevation of systemic blood pressure. It is suggested that an increased concentration of vasodilator PLS during TBP may contribute to the hypotension observed in total body perfusion.

The Effect of Prostaglandins F2α And E2 on Pregnancy in Mice During Implantation

The uterine content of prostaglandins (PGs) increases following insertion of an intrauterine device (IUD). Such IUD-bearing uteri also exhibit impaired decidualization. Although prostaglandins have been shown to be luteolytic in several species, it is not clear that inhibition of decidualization is mediated solely through alterations in ovarian steroidogenesis. In these experiments, ovariectomized, hormone-replaced pregnant mice, as well as intact mice, were treated systemically with either PGE2 or PGF2alpha so that the extraovarian actions of prostaglandins upon decidualization could be segregated from effects mediated by alterations in ovarian steroidogenesis. The results suggest that the effect of PGF2alpha upon decidualization was mediated via an alteration in ovarian steroidogenesis, but that PGE2 acted independently of the ovary. The hypothesis is presented that alterations in the ratio of E to F prostaglandins elicited within the endometrium by an IUD inhibit decidualization at the uterine level, and that this effect might be mediated by impairment of histamine release from endometrial mast cells.

Effects of cervical sympathetic ganglionectomy on cyclic-amp and prostaglandins in brain and eye tissues and fluids

Studies were conducted confirming supersensitivity to catecholamines on intraocular pressure and pupil size following bilateral superior cervical ganglionectomy in rabbits. At the termination of these studies we examined changes in cyclic adenylic acid and prostaglandin content in jugular vein effluent and various brain and ocular tissues and fluids of the sympathectomized versus control animals. In the blood effluent and various brain and ocular tissues and fluids of and significant lowering of prostaglandin F1 α in the sympathectomized animals. Although we found elevation of prostaglandin in certain tissues of the sympathectomized animals, there were no significant changes in cyclic adenylic acid levels between sympathectomized and control animals in the tissues examined. The findings of prostaglandin (blood and tissue) and cyclic adenylic acid (blood) changes in sympathectomized animals, associated with known changes in intraocular pressure and pupil size (due to catecholamine supersensitivity) must elicit further interest in the correlation and interpretation of various other central physiological and metabolic events in cervical sympathectomized animals.

Prostaglandin e production by cultured inflamed rat synovium; stimulation by colchicine and inhibition by chloroquine

Acute arthritis was induced by injection of cell-free extract of group A type 4 Streptococci, into the knee joints of three month old male rats. Slices of the inflamed synovium obtained from these rats were incubated for 60–240 minutes, and the rate of prostaglandin E accumulation in the medium was measured by radioimmunoassay.Prostaglandins of the E type accumulated in the medium at a near linear rate during the incubation of the inflamed synovium for 4 hours. Incubation of inflamed synovium in the presence of colchicine (10 μg/ml) brought about a two-fold increase in the prostaglandin E accumulation in the medium after a latency of one hour. Tissue content of prostaglandin E after 4 hours of incubation of inflamed synovium with colchicine doubled as well. In contrast, incubation of inflamed synovium with chloroquine (10 μg/ml), corticosterone or dexamethasone (100 μg/ml each) reduced prostaglandin E accumulation in the medium by 50% at 1–4 hours. Likewise, chloroquine, corticosterone or dexamethasone reduced the tissue content of prostaglandin E in the inflamed synovium after 4 hours of incubation. The suppressive action of chloroquine was prevented by addition to the medium of arachidonic acid (2 μg/ml). It is concluded that the anti-inflammatory properties of colchicine are probably not related to prostaglandin biosynthesis. On the other hand chloroquine exerts its anti-inflammatory properties by curtailing substrate availability (arachidonic acid) for prostaglandin production, similarly to the anti-inflammatory mechanism of steroid hormones.