{"title":"Monthly prostaglandin bibliography prepared by the University of Sheffield Biomedical Information Service.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"45 2","pages":"B10-21"},"PeriodicalIF":3.0,"publicationDate":"1992-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12729112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Monthly prostaglandin bibliography prepared by the University of Sheffield Biomedical Information Service.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"44 1","pages":"B1-12"},"PeriodicalIF":3.0,"publicationDate":"1991-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13105942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y. Sakagami, Y. Mizoguchi, S. Seki, K. Kobayashi, S. Morisawa, S. Yamamoto
{"title":"Release of leukotriene B4 from rat Kupffer cells.","authors":"Y. Sakagami, Y. Mizoguchi, S. Seki, K. Kobayashi, S. Morisawa, S. Yamamoto","doi":"10.2957/kanzo.29.753","DOIUrl":"https://doi.org/10.2957/kanzo.29.753","url":null,"abstract":"In order to examine the production of leukotriene B4 (LTB4) from Kupffer cells, Kupffer cells isolated from the normal rat liver were incubated with calcium ionophore A23187, opsonized zymosan, or platelet activating factor (PAF), and the amount of LTB4 in the culture supernatant was determined by the combined technique of reverse-phase high-performance liquid chromatography and radioimmunoassay. As a result, when activated in vitro with calcium ionophore A23187, Kupffer cells generated LTB4. When Kupffer cells were stimulated with calcium ionophore after 10-min preincubation with AA861, a selective 5-lipoxygenase inhibitor, the release of LTB4 from Kupffer cells was markedly suppressed. PAF, which is a phospholipid mediator having a wide spectrum of biological activities, significantly enhanced the release of LTB4 from Kupffer cells stimulated with calcium ionophore or opsonized zymosan. Even when the Kupffer cell were not stimulated with calcium ionophore or opsonized zymosan, LTB4 production was significantly increased by PAF. Thus, our studies indicate that Kupffer cells could generate LTB4 as well as polymorphonuclear leukocytes and macrophages. In addition, it is suggested that Kupffer cells may be able to modify inflammatory and immunological events in the liver tissue by the release of LTB4.","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"77 1","pages":"125-8"},"PeriodicalIF":3.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86883724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ultrastructural autoradiographic localization of exogenous arachidonic acid in cultured endothelial and smooth muscle cells.","authors":"S I Tasca, Z Galis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The uptake and intracellular localization of exogenous arachidonic acid (AA) were investigated in cultured endothelial (EC) and smooth muscle cells (SMC) isolated from bovine aorta. The [14C]AA uptake was assessed biochemically and by light and electron microscopic autoradiography. The highest values of silver grain surface density were associated with the mitochondria, lysosomes, and the Golgi apparatus of the EC. The grain linear density was greater on the nuclear envelope than on plasmalemma. On SMC, the grain density was highest on lipid droplets whereas the linear densities of the nuclear envelope and plasmalemma were similar. The share of each subcellular compartment in the AA distribution was estimated as the percentage of the individual silver grain count out of the total cell-associated radioactivity. The results showed that cytoplasm (including endoplasmic reticulum, ribosomes, and small vesicles) made the main contribution followed by the nucleus and at lower values by other organelles. These subcompartments may represent the intracellular sites from which AA could be mobilized for prostanoid synthesis by EC and SMC.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"165-71"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14272273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Assessment of plasma leukotriene and prostaglandin levels during adjuvant arthritis and kaolin-induced paw oedema in rats.","authors":"M Melli","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Plasma levels of some arachidonic acid metabolites were investigated in acute and chronic models of inflammation in rats. As a model of chronic inflammation, adjuvant arthritis in rats induced by the injection of Freund's complete adjuvant, and as an acute model for inflammation, kaolin-induced paw oedama were used. Plasma leukotriene(LT) C4-like and prostaglandin(PG) E2-like activities were quantitated by bioassay in guinea-pig ileum and rat stomach fundus respectively. In the course of adjuvant arthritis, plasma levels of LTC4- and PGEi2-like activities were increased. Plasma LTC4-like activity reached a maximum within 3 weeks, while PGE2-like activity reached a maximum 10 days after adjuvant injection. In the early phase of adjuvant arthritis, levels of both LTC4- and PGE2-like activities were found to be low but both activities were increased in the late phase of inflammation.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"173-8"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14316987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pharmacological management of an impending placental insufficiency.","authors":"H Köpernick, H J Mest, B Schwarz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>By means of drug administration a further decrease of the placental circulation in premature sonographic maturity of the placenta could be prevented via influencing the TXA2/PGI2 balance. Treatment of premature sonographic placental maturity with 50 mg acetylsalicylic acid (ASA) per day and three times daily 100 mg Rocornal, respectively, resulted in a significant increase of the birth weights. In a second series of experiments, three groups were treated with 50 mg/day ASA or 250 mg ASA/once per week and three times/day 100 mg Rocornal, respectively, from the 18th or 20th week of gestation to the 35th week. Subsequently, they were compared to a group of untreated controls. The birth weights of all treated groups were statistically significantly higher. The underlying mechanism is suggested to be an improved microcirculation.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"179-83"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14187335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of essential fatty acid deficiency on renal papillary lipid methylation.","authors":"R F O'Dea, T P Green, A R Sinaiko","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The relationship between lipid methylation and prostaglandin release was examined in rat renal papillae. Essential fatty acid deficiency (EFAD) was produced to deplete tissues of arachidonate precursors. The in vitro release of prostaglandin E was determined after exposure of the papillae to hypertonic sodium chloride. The EFAD animals were observed to have significantly less renal papillary lipid methylation than rats fed control diets (50%; P less than 0.05). However, stimulation of prostaglandin production in vitro was not accompanied by any detectable changes in total lipid methylation in tissues from either normal or EFAD rats.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"199-202"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14316989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
V Mohsenin, P G Tremml, K G Rothberg, M Souhrada, J S Douglas
{"title":"Airway responsiveness and prostaglandin generation in scorbutic guinea pigs.","authors":"V Mohsenin, P G Tremml, K G Rothberg, M Souhrada, J S Douglas","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Airway responsiveness to histamine aerosol and lung prostaglandin generation were investigated in normal, partially vitamin C deficient and scorbutic guinea pigs. The ascorbic acid content of the lung expressed as microgram/100 mg wet weight lung parenchyma decreased from 22.1 +/- 1.8 (mean +/- SE) in the control group to 9.0 +/- 1.4 and 1.8 +/- 0.4 in tissues from partially ascorbic acid deficient and scorbutic animals, respectively. Guinea pigs on low and ascorbic acid deficient diets developed significant airway hyperresponsiveness to histamine aerosol after 3 and 4 weeks. Indomethacin (30 mg/Kg, i.p.) further increased the airway hyperresponsiveness in scorbutic animals but was without effect in control animals. Prostaglandin generation from different parts of the lung was significantly changed by the diets. However, airway hyperresponsiveness was not directly attributable to altered prostanoid generation. Scorbutic conditions did not alter the electrophysiological characteristics of airway smooth muscle namely, resting membrane potential and electrogenic sodium pump activity. In summary, ascorbic acid deficiency causes airway hyperresponsiveness to histamine in guinea pigs. This alteration seems not to be related to an altered prostaglandin generation by the lung or to the electrophysiological properties of airway smooth muscle.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"149-55"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14316984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R N Goldberg, C Suguihara, O Martinez, A Bancalari, M R Clark, E Bancalari
{"title":"The role of leukotrienes in the late hemodynamic manifestations of group B streptococcal sepsis in piglets.","authors":"R N Goldberg, C Suguihara, O Martinez, A Bancalari, M R Clark, E Bancalari","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In order to evaluate the role of leukotrienes in group B streptococcal (GBS) sepsis we studied the effect of a leukotriene receptor antagonist, FPL 57231, on the late hemodynamic changes occurring secondary to an infusion of live GBS. Paralyzed, mechanically ventilated piglets received a continuous intravenous infusion of bacteria (5 x 10(7) org/kg/min) while systemic arterial (Psa) and pulmonary artery pressures (Ppa) were measured. To separate the effects of the lipoxygenase products of arachidonic acid from those of the cyclooxygenase by-products, animals in control and treatment groups received indomethacin, a cyclooxygenase blocking agent, 15 min after the infusion of GBS was begun. In addition to GBS and indomethacin, treatment animals received a 30 min infusion of FPL 57231 starting 120 min after the bacterial infusion was begun. All study animals responded to bacteria within 15 min with marked elevation in pulmonary artery pressure (X +/- SD) (12 +/- 3 to 49 +/- 5 mmHg; p less than .01), and a decline in PaO2 (84 +/- 9 to 49 +/- 5 mmHg; p less than .01) and cardiac output (0.29 +/- 0.04 to 0.18 +/- .07 liter/min/kg; p less than .01). These changes were reversed by indomethacin. Subsequent values remained relatively stable until approximately 90 min when a gradual decrease in cardiac output (CO) and PaO2, and an increase in Ppa, and calculated systemic (SVR) and pulmonary (PVR) vascular resistances occurred. After the initial increase in TxB2 and 6-keto-PGF1 alpha, indomethacin treatment resulted in return of these values to baseline with no further increase throughout the study period.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"191-8"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14187336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A possible mechanism of airway hyperresponsiveness induced by prostaglandin F2 alpha and thromboxane A2.","authors":"H Aizawa, T Hirose","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To elucidate the precise mechanisms of airway hyperresponsiveness induced by prostaglandin F2 alpha (PGF2 alpha) and thromboxane A2 (TXA2), we investigated the effects of the subthreshold dose (the highest dose which does not lead to contraction) of PGF2 alpha and stable TXA2 analogue, STA2 (epithiomethano-TXA2), on the smooth muscle contraction evoked by acetylcholine (ACh) and electrical field stimulation (EFS) in the canine trachea. These prostanoids produced no changes in the contractile response to both these stimuli. Thus, neither PGF2 alpha nor TXA2 affect the smooth muscle, as the site of action for ACh is the muscarinic receptor located on smooth muscle. Neither compound affect the postganglionic vagal efferent nerve, because the EFS contracts smooth muscle via activation of the postganglionic vagal efferent neuron. This study, together with our previous observation, suggests that PGF2 alpha and TXA2 induce airway hyperresponsiveness by stimulating vagal sensory endings and by activating the reflex pathway.</p>","PeriodicalId":20659,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"33 3","pages":"185-9"},"PeriodicalIF":3.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14316988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}