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PubMed1988

Structure requirements for antiproliferative and cytotoxic activities of marine coral prostanoids from the Japanese stolonifer Clavularia viridis against human myeloid leukemia cells in culture.

The structural requirements for antiproliferative and cytotoxic activities of marine coral prostanoids from Japanese stolonifer Clavularia viridis and related compounds were examined in HL-60 cells in culture. From our data on the structure-activity relationship of these compounds, we elucidated that 1) the alkylidenecyclopentenone structure in these prostanoids was required for the antiproliferative and cytotoxic activities against HL-60 cells, but the epoxy prostanoids without cross-conjugated cyclopentenone system had the activities; 2) the presence of hydroxyl group at C-12 position in the prostanoids enhanced the activities, but the stereospecificity of the 12-hydroxyl group was not required for the activities; 3) the introduction of halogen atom at C-10 position of the prostanoids potentiated the activities (Cl greater than Br = I greater than H); 4) the introduction of blocking groups for blocking beta-oxidation to the alpha-side chain of the prostanoids did not cause the marked increase of the activities; 5) the presence of dienone (C5-6 and C7-8) in the structure potentiated the activities. These results provide the basis for drug-design of a new class of antitumor agent from marine coral prostanoids.

Animals↗
PubMed1989

Influence of iloprost on eicosanoid generation and lipid levels in experimental myocardial ischemia in dogs.

Anaesthetized mongrel dogs were subjected to occlusion of a coronary artery. The resulting myocardial infarction was observed for three hours. One hour after occlusion, infusion of the stable prostacyclin analogue iloprost or saline was started. In the control group myocardial infarction was associated with an increase of the ratio TXB2/6-keto-PGF1a which was abolished by iloprost treatment. After occlusion in the control group, the atherosclerosis index (TC-HDLC): HDLC was increased, but in the iloprost-treated group it was significantly decreased. The results of this study suggest that the administration of iloprost is able to prevent changes in eicosanoid metabolism and lipoprotein pattern after coronary artery occlusion in dogs.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Vasopressin-stimulated water flow is decreased by thromboxane synthesis inhibition or antagonism.

The time course of vasopressin stimulation of water flow and immunoreactive thromboxane B2 (iTXB2) and prostaglandin E (iPGE) biosynthesis was studied in the isolated toad urinary bladder. Vasopressin (25 mU/ml) significantly stimulated iTXB2 synthesis within 8 min, synthesis reaching a maximum rate by 17 min. iPGE synthesis was significantly stimulated within 8 min, remaining unchanged for 24 min. Maximum vasopressin-stimulated water flow was reached between 16 and 24 min. 7-(1-Imidazolyl)-heptanoic acid (7IHA), a thromboxane synthetase inhibitor, inhibited both vasopressin-stimulated water flow and iTXB2 synthesis in a dose-dependent fashion, but did not affect iPGE synthesis. Vasopressin-stimulated water flow and iTXB2 synthesis were significantly correlated (r = 0.75, n = 24, P less than 0.001). 13-Azaprostanoic acid (13APA), a thromboxane antagonist, inhibited vasopressin-stimulated water flow in a dose-dependent fashion. Inhibition of arachidonic acid metabolism abolished the effects of 7IHA and 13APA on vasopressin-stimulated water flow. 7IHA and 13APA had no effect on cAMP-stimulated water flow. These results confirm that vasopressin stimulates TXA2 and PGE synthesis and support the hypothesis that TXA2 is a positive modulator of vasopressin-stimulated water flow in the toad urinary bladder.

Animals↗
PubMed1988

Alterations in rabbit renal microvascular prostanoid synthesis in acute renal failure.

Vasodepressor prostanoids have been suggested to regulate renal hemodynamics after nephrotoxic injury and thus protect the kidney against the effects of prolonged ischemia. This study assessed whether changes in two microvascular vasodilator prostanoids would correlate with changes seen in renal hemodynamics in rabbits with nephrotoxic renal injury produced by either uranyl nitrate or mercuric chloride. Rabbits were killed at 3, 24, and 72 h after the nephrotoxin injections and 6-ketoprostaglandin (PG) F1 alpha and PGE2 synthesis was measured in vitro in isolated renal microvessels. At the end of 24 h, synthesis of both prostanoids was significantly increased in all nephrotoxin-treated animals, an observation not noted at the end of 3 h. At 72 h, 6-keto-PGF1 alpha production remained elevated. Pretreatment with mepacrine blocked the increased prostanoid production seen in uranyl nitrate-treated animals. Thus, renal microvascular vasodilator prostanoid biosynthesis is increased 24-72 h after nephrotoxin administration. These data suggest that the biosynthesis of prostacyclin and PGE2 may contribute to the maintenance of renal blood flow in the first few days after acute renal injury and further suggest that a mechanism for this increase may be stimulation of phospholipase A2.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Role of glomerular prostanoid in control of glomerular filtration rate in rats.

It is generally accepted that the main action of glomerular prostanoids (GPs) on glomerular filtration rate (GFR) is to modulate the activity of different vasoconstrictors, specially in states of renal hypoperfusion. However it was also suggested that GPs may directly affect GFR. The present study was focused on this last hypothesis, in different experimental models, in rats. In adriamycin induced acute renal failure, the transient decrease of GFR is associated with higher levels of thromboxane B2. Later on, when GFR returns to normal, vasodilator prostaglandins synthesis was also increased. In captopril induced renal failure in Na depleted rats (where GPs synthesis remained normal), stimulation of PGE2 and PGI2 production by K and NaCl was associated with a significant improvement of GFR. Furthermore, the increase in GFR induced by NaCl was prevented by inhibition of prostaglandin synthesis. Infusion of atrial natriuretic peptide in euvolemic rats induce a marked elevation both of GFR and PGE2 synthesis. It was abolished by previous administration of prostaglandin synthesis inhibitor. In conclusion, glomerular prostanoids may influence GFR, either directly, or as mediator or modulator of other vasoactive hormones.

Acute Kidney Injury↗
PubMed1982

Profiles of prostaglandin metabolites in the human circulation. Identification of late-appearing, long-lived products.

The pattern of metabolites appearing in the circulation after intravenous injection of [9 beta-3H]prostaglandin F2 alpha was investigated in the human. Analysis of profiles of products was performed by two-dimensional TLC and autoradiography. Identification of labeled metabolites was accomplished by comparing their chromatographic behaviour with reference compounds in several chromatographic systems. After injection of [9 beta-3H]prostaglandin F2 alpha the initially formed metabolite was 15-keto-13,14-dihydroprostaglandin F2 alpha. However, this compound only dominated the spectrum of metabolites during the first few minutes, and several more polar products soon appeared. About 20 min after the injection the most prominent metabolite was 5 alpha, 7 alpha-dihydroxy-11-ketotetranorprostane-1,16-dioic acid, which remained the dominating plasma compound and was also the major metabolite in urine. Several other highly oxidized products were also identified in plasma. Also these metabolites appeared later and remained longer in the circulation than the initially formed 15-ketodihydro metabolite. Our findings suggested that the more degraded metabolites might serve as more reliable plasma parameters for monitoring prostaglandin production than the traditional parameter, 15-ketodihydroprostaglandin F2 alpha. This hypothesis was supported by radioimmunoassay of metabolite levels in plasma appearing after either exogenous (intravenous administration) or endogenous prostaglandin F2 alpha (late human pregnancy and parturition). In all cases studied, the tetranor metabolites remained elevated in the circulation for several hours, in contrast to their precursor, 15-ketodihydroprostaglandin F2 alpha, which disappeared rapidly.

Autoradiography↗
PubMed1988

Arachidonate metabolism in myocardial ischemia and reperfusion.

Circulatory blood corpuscles have enzymes catalyzing arachidonic acid. Platelets have cyclo-oxygenase system which produce highly vasoconstrictive and thrombogenic thromboxane A2 (TXA2). Neutrophils have another type of arachidonate metabolism system, lipoxygenase enzymes, which produce hydroxyeicosatetraenoic acids (HETE) and leukotrienes (LT), mediating inflammatory reactions. These arachidonate metabolites were found to play important roles in the evolution of myocardial ischemia. Thromboxane B2 (TXB2) a stable metabolite of TXA2, was elevated in peripheral blood of patients with angina pectoris. This elevation of TXB2 was supposed to be derived from platelet activation in coronary circulation due to altered production of TXA2 and prostacyclin (PGI2). Augmentation of TXA2 was also observed in patients with acute myocardial infarction. TXA2 synthetase inhibitors decreased plasma levels of TXB2 in these patients accompanied by attenuation of infarct size. Neutrophils were found to accumulate in ischemic myocardium and were augmented at reperfusion phase especially at interface between infarcted and risk zone. These infiltrated neutrophils may also provide deleterious effects on myocardial cells by producing lipoxygenase metabolites. In fact, a chemotactic and vasoconstrictive lipoxygenase product, 12-HETE, was produced selectively in ischemic myocardial tissue of an occlusion-reperfusion model. During evolution of myocardial cell damage, platelets and neutrophils, accumulated in ischemic tissue, may contribute to the exacerbation of microcirculatory disorders by producing vasoactive prostanoids, leading to expansion of myocardial necrosis. We should gain insights into these cellular interactions through arachidonate metabolism under normal and catastrophic conditions of coronary circulation.

Arachidonic Acids↗
PubMed1976

Metabolism of PG in man: effect of furosemide on the excretion of the main metabolite of PG F2alpha.

The excretion rates of main urinary metabolite of PG F2alpha were measured radioimmunologically in 4 healthy persons and in 13 essential hypertensives. The resting values were 9.3+/-0.73 in the former and 10.4+/-2.17 ng/min in the latter. There was no significant differences between them. The excretion of the metabolite decreased prominently after the administration of furosemide. The percent decrease was 57% in healthy persons and 70% in essential hypertension. The percent result supports that furosemide inhibit the catabolism of PG F2alpha.

Depression, Chemical↗
PubMed1982

A single platelet aggregometric assay for pro-and antiaggregatory prostanoids.

A method is described for characterizing disaggregatory and proaggregatory prostanoids in a single assay. This "post-addition assay" consists of adding the test agent to PRP containing PGI2 (4-6 nM) 90 sec after an ADP challenge. The relative potencies of known inhibitors of ADP-induced aggregation were identical to the relative disaggregatory potencies determined by post-addition. The proaggregatory relative potencies for 16, 16-Me2-PGE2,PGE2,PGH2 and 11 alpha,9 alpha-epoxymethano-15 alpha-hydroxy-prostadienoic acid were 5.8 :2 : 1.8 : 1, respectively, revealing the significant thrombosis promoting activity of PGE2 and its analogs.

Adenosine Diphosphate↗
PubMed1988

Short- and long-term treatment with rosaprostol of patients with gastritis.

Therapy with rosaprostol was applied in 25 patients with gastritis, namely 11 cases for about 30 days and 14 for 60 days, without further gastro-protective treatments. The drug induced an early complete disappearance of subjective and objective symptoms, already at the end of the first ten days of treatment, whereas the endoscopic and the histological findings revealed a highly significant improvement at the end of the treatment, with normalization in nearly all the cases. The drug was well tolerated, and did not induce diarrhoea nor change haemodynamic parameters. These highly significant results emphasize the efficacy and safety of the drug.

Adult↗
PubMed1984

The influence of ultraviolet B irradiation on the excretion of the main urinary metabolite of prostaglandin F1 alpha and F2 alpha in psoriatic and normal subjects.

The influence of ultraviolet B (UVB) irradiation on the excretion of the main urinary metabolite of prostaglandin F1 alpha and F2 alpha (PGF-MUM) in 7 normal male volunteers and 7 male patients with stable psoriasis was examined. The excretion of PGF-MUM was increased during the first 24 hours after UVB irradiation of back skin and was generally reduced to near pre-irradiation levels during the next 24 hours after irradiation, in both normal and psoriatic subjects. Although pre-irradiation levels of PGF-MUM excretion in psoriatic patients were lower than those in normal subjects as previously reported, it was demonstrated that PGF-MUM excretion after UVB irradiation in psoriatic patients was fairly increased and amounted to near the mean pre-irradiation level in normal subjects. These results suggested not only a disorder in endogenous prostaglandin synthesis in psoriatic patients but a considerable capacity of psoriatic skin to synthesize prostaglandin after UVB irradiation.

Adult↗