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PubMedDate not supplied

Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate.

In helically cut strips of dog cerebral, coronary, mesenteric and femoral arteries, the contractile response to prostaglandin (PG) F2alpha, and E2, relative to contractions induced by 30 mM K+, did not appreciably differ, whereas relaxations induced by PGE1 relative to those induced by 10(-4) M papaverine were significantly different; the least in cerebral arteries and the greatest in mesenteric arteries. The relaxation of human cerebral arteries in response to PGE1 was similar to that of dog cerebral arteries. Treatment for 60 min with polyphloretin phosphate (3 X 10(-5) and 10(-4) g/ml) suppressed the contractile response to PGF2alpha and E2 but did not alter the response to 25 mM K+. The relaxing effect of PGE1 was not influenced. Aspirin (5 X 10(-5) and 2 X 10(-4) M) significantly potentiated the contractile response to PGF2alpha and E2 but did not alter the relaxation induced by PGE1. In contrast, contractions induced by serotonin were attenuated. It is concluded that dog cerebral, coronary, mesenteric and femoral arteries relaxed differently in response to PGE1. It appears that arterial responses to vasoconstricting PGs, but not to the vasodilating PG, are significantly attenuated by polyphloretin phosphate and potentiated by aspirin.

Aged↗
PubMed1990

Polyphloretin phosphate (PPP) antagonists of prostaglandin action also inhibit prostaglandin biosynthesis in-vitro.

Several polyphloretin phosphate (PPP) fractions (low mol. wt LC1259; high mol. wt LC1261; crude mixture, LC101) were confirmed in their established property as antagonists of the pharmacological actions of prostaglandins in a preparation of guinea-pig isolated ileum stimulated by prostaglandin (PG)E2. Further samples of the same material were then compared in-vitro with indomethacin in their ability to inhibit prostaglandin biosynthesis from arachidonic acid by a microsomal enzyme preparation. All three PPP fractions potently inhibited prostaglandin generation, with the rank order of potency LC1259 = LC101 = indomethacin greater than LC1261. The oral LD50 in mice was 25 mg kg-1 for indomethacin and greater than 1 g kg-1 for LC101. PPP fractions (especially LC101) may therefore have therapeutic potential as anti-inflammatory agents.

Animals↗
PubMed1984

Antagonistic effect of polyphloretin phosphate and di-4-phloretin phosphate on the contractile responses of guinea-pig gastric muscles to prostaglandin E2.

Polyphloretin phosphate (PPP) and di-4-phloretin phosphate (DPP) were studied for their ability to antagonize the contractions produced by prostaglandin E2 (PGE2) on isolated guinea-pig gastric muscles. PPP (100, 200 and 300 micrograms/ml) and DPP (10, 30 60 and 100 micrograms/ml) inhibited reversibly the PGE2-produced excitatory effect in longitudinal fundus and corpus muscles but did not influence the PGE2-produced inhibitory effect in circular muscle strips. In the presence of PPP and DPP the concentration-effect curves for PGE2 were shifted to the right parallel to control curves. The antagonistic action of PPP and DPP appeared to be a specific one since the compounds had little, if any, effect on the responses to histamine, acetylcholine and BaCL2. Analysis of the data (1) showed that DPP is a more potent antagonist than PPP against PGE2 on guinea-pig gastric muscle with pA2 6,1 and 4,8, respectively.

Animals↗
PubMed1978

The character of the antagonism by polyphloretin phosphate of contractions to prostaglandins E1 and F 2alpha in guinea-pig ileum.

Polyphloretin phosphate (PPP) produced a dose-dependent decrease in the tone and reduction of the spontaneous phasic contactions of the longitudinal muscle of guinea-pig isolated ileum. PPP (100 microgram ml-1) after a 2 min contact with the ileum decreased the contractile effects of PGE1 0.1 micron by 40.6 +/- 7.4%, of PGE1 0.01 micron by 86.7 +/- 3.3% and of PGE2alpha 0.1 micron by 62.2 +/- 8.6%. After 10 min contact of PPP the contractile effect of PGE1 0.1 micron was decreased by 47.7 +/- 4.7% and that of PGE2alpha 0.1 micron by 89.6 +/- 1.7%. When the contact was longer, PPP showed a pronounced after-effect in respect to the effects of PGE1 and particularly of PGF2alpha. PPP signicantly reduced contractions to 5-HT and BaCL2, but not to acetylcholine, histamine or substance P. The type of antagonism of PGE1 by PPP was examined using cumulative concentration-effect curves for PGE1 in the presence of increasing concentrations of PPP. We conclude that on guinea-pig ileum PPP acts as a non-competitive antagonist of PGE1 and PGF2alpha.

Acetylcholine↗
PubMed1975

An inhibitory effect of polyphloretin phosphate (PPP) on local anaesthesia.

In the present investigation it is shown that administration of polyphloretin phosphate (PPP) together with local anaesthetics decreased the duration of infiltration anaesthesia in guinea-pigs. Furthermore, it is shown that in infiltration anaesthesias the local anaesthetic effect was terminated within a few minutes by administration of PPP. In experiments with high- and low-molecular fractions of PPP, the "anti-local anaesthetic" effect of PPP was not due to the antiprostaglandin activity of PPP. There was no effect of PPP on the duration of the nerve-blocking activity of mepivacaine in rats. Neither did the administration of PPP influence the toxic effects of mepivacaine in rabbits.

Anesthesia, Local↗
PubMed1978

Influence of polyphloretin phosphate on the central effects of prostaglandin E2 and F2alpha in rats.

The possibility that polyphloretin phosphate (PPP) antagonizes the central effects elicited by prostaglandin (PG) E2 and F2alpha was investigated. PPP was administered i.c.v. to male Wistar rats (10 or 25 microgram) 10 or 30 min before i.c.v. injection of PGF2 or PGF2alpha (1 or 10 microgram). The duration of several component of behavior, the degree of irritability, and the rectal temperature of rats were measured; the levels of noradrenaline, dopamine, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid were measured spectrophoto-fluorometrically in discrete brain areas. PPP antagonized temperature and behaviroal changes induced in rats by PGF2alpha, but not those induced by PGE2. The magnitude of antagonism depended on the dose of PPP and on the time of the pretreatment before PGF2alpha administration. Changes in the level of biogenic amines in discrete brain areas evoked by PGs were not affected by PPP. We found that PPP antagonizes the central effects of PGF2alpha but not those of PGE2, and that changes of biogenic amines in discrete brain areas elicited by PGs are not specific.

Animals↗
PubMedDate not supplied

Central action of low-molecular weight polyphloretin phosphate fraction in rats.

The central effects of a low-molecular weight fraction of polyphloretin phosphate (PPP) with molecular weight about 4600 were studied using several behavioural tests in animals (Lat's test, open-field test, hold-board test, irritability, spontaneous motor activity), chlorpromazine-induced catalepsy test, body temperature measurements, hexobarbital-induced sleep duration, reaction to thermal painful stimulus, measurements of arterial blood pressure, heart rate and respiratory rate. The activity of prostaglandin synthetase was determined also in the microsomes of bovine hypothalamic cells in vitro. Using some of the above tests the effect of PPP was studied on the central action of prostaglandins F2 alpha and E2 (PGF2 alpha and PGE2). PPP was administered intraventricularly (i.c.v.) in various doses (doses producing the lowest pharmacological effect in a given test) 10 minutes before i.c.v. administration of these prostaglandins in doses of 1 or 10 microgram. It was shown that PPP (low-molecular weight fraction) injected into the lateral cerebral ventricle of the rat exerted a biological effect on the central nervous system manifesting itself as behaviour changes in the tests used, and as changes of the arterial blood pressure. PPP i.c.v. antagonized certain central effects of PGF2 alpha and PGE2. The degree of inhibition of various prostaglandins differed in relation to the test used and was somewhat stronger in the case of PGF2 alpha.

Animals↗
PubMed1985

Polyphloretin phosphate, an antagonist of thyrotropin action: evidence for an interaction with the hormone rather than the receptor.

Polyphloretin phosphate (PPP) is known to be an inhibitor of bovine TSH (bTSH)-induced stimulation of the thyroid in both in vivo and in vitro assays. The present studies were undertaken to delineate the mechanism of these effects. A high molecular weight PPP preparation strongly inhibited both the binding of 125I-labeled bTSH [( 125I]bTSH) to human thyroid membranes and the stimulation of adenylate cyclase evoked by bTSH therein. Inhibition of bTSH-induced adenylate cyclase activity by PPP was evident both in the absence and the presence of NaCl (150 mM) in the incubation medium. Incubation of membranes with PPP, followed by its removal, did not affect subsequent binding of [125I]bTSH, indicating that PPP did not bind firmly to or damage the TSH receptor. Gel chromatography on Sephadex G-100 revealed that [125I]bTSH incubated with PPP eluted earlier than [125I]bTSH alone, indicating that PPP had formed a higher molecular weight complex with [125I]bTSH. This effect could be prevented by the addition of an excess of unlabeled bTSH to the incubation mixture. Binding of [125I] bTSH in the higher molecular weight peak generated by incubation with PPP was less than half that in control specimens of [125I]bTSH. Studies with PPP were also conducted in a highly sensitive assay that employs cultured porcine thyroid cells and measures the cAMP response induced by bTSH. The inhibitory effect of PPP on bTSH-induced cAMP accumulation was also evident in this assay. However, the presence of divalent cations Ca++ and Mg++ in the assay medium greatly diminished the inhibitory effect of PPP. Similarly, addition of Ca++ and Mg++ to the incubation medium greatly reduced or abolished the inhibitory effect of PPP on [125I]bTSH binding. Both effects of these salts to lessen the inhibitory response to PPP were overcome by increasing the PPP concentration. Gel chromatographic studies revealed that Ca++ and Mg++ acted by inhibiting the formation of the high molecular weight complex of bTSH and PPP. From these findings, we conclude that PPP exerts its inhibitory effect on TSH-induced stimulatory responses in the thyroid, in vivo as well as in vitro, by forming a complex with the hormone. The complex either does not bind to TSH receptors or does so with much lower affinity.

Adenylyl Cyclases↗
PubMed1976

Inhibitory actions of polyphloretin phosphate and related compounds on the response to prostaglandin in the smooth muscle of guinea-pig stomach.

The inhibitory actions of polyphloretin phosphate (PPP) and related compounds, di-4-phloretin phosphate (DPP), PHLORETIN AND TRIHYDROXY PROPIOPHENONE (THPP) on the contractile responses to prostaglandin (PG) and acetylcholine (ACh) in longitudinal smooth muscle of guinea-pig stomach were studied. Of the four inhibitors PPP and DPP showed relatively selective antagonism for PGE1. DPP gave the highest pW2 value against PGE1. These results indicate that DPP is a useful antagonist of PG in smooth muscle, although it slightly inhibits responses to ACh, 5-HT or histamine, and the Ca-induced contracture in K depolarized preparation.

Acetylcholine↗
PubMed1979

The prostaglandin antagonist polyphloretin phosphate behaves as a nonspecific inhibitor of rat hepatic adenylate cyclase.

The mechanism of the nonspecific inhibitory effects of the prostaglandin antagonist polyphloretin phosphate (PPP) was studied on a partially purified adenylate cyclase preparation from rat livers, PPP in concentrations above 100 micrograms/ml reduced the enzyme activity below basal values regardless of the stimulator used. The activity of adenylate cyclase in a persistent active state due to enzyme preincubation with guanylylimidodiphosphate (Gpp(NH)p) was inhibited 5-10 times more weakly. Kinetic studies indicate that PPP does not influence directly the catalytic site for ATP. PPP seems to produce permanent enzyme inhibition which is not antagonized by repeated washing ot the enzyme preparation. The reduced catalytic activity of adenylate cyclase retains after treatment with PPP the character of its responsiveness to the stimulators, which depends on the state of the enzyme before exposure to the inhibitor.

Adenylyl Cyclase Inhibitors↗
PubMed1975

Reduction of the tone of the isolated human umbilical artery by indomethacin, eicosa-5,8,11,14-tetraynoic acid and polyphloretin phosphate.

The effects of 2 prostaglandin synthetase inhibitors, indomethacin and eicosa-5,8,11,14-tetraynoic acid (ETA) and of the prostaglandin antagonist, polyphloretin phosphate (PPP), on the tone of the isolated human umbilical artery and on the responses of this preparation to 5-hydroxytryptamine (5-HG) and prostaglandin F2alpha (PGF2alpha) were investigated. Indomethacin (8 mug/ml), ETA (5 mug/ml) or PPP (40 mug/ml) reduced the tone of human umbilical arteries but had no influence on the responses to 5-HT. In these concentrations ETA and PPP but not indomethacin antagonized the action of PGF2alpha. When the concentration of indomethacin or PPP was increased 5-fold both 5-HT- and PGF2alpha-induced contractions were antagonized indicating a non-specific inhibition at these concentration levels. A 10-fold increase in the concentration of ETA had no antagonizing action on 5-HT-induced contractions suggesting a more selective inhibition of the PGF2alpha action than displayed by the other compounds. The effects on the tone of the human umbilical artery of the compounds studied might reflect inhibition of prostaglandin biosynthesis and/or antagonism of the action of formed prostaglandins. The findings are compatible with the view that intramural synthesis of prostaglandins contributes to the maintenance of the tone of the isolated human umbilical artery.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1975

7-oxa-13-prostynoic acid and polyphloretin phosphate as non-specific antagonists of the stimulatory effects of different agents on adenylate cyclase from various tissues.

7-oxa-13-prostynoic acid (OPA) and polyphloretin phosphate (PPP) are believed to act as specific antagonists of prostaglandin action. In order to estimate their specificity, the inhibitory effects of these drugs were tested on the activity of adenylate cyclase from several tissues which were stimulated by prostaglandins and several other compounds. In adenylate cyclase preparation from L-fibroblasts both OPA (0.15-1.5 MM) and PPP (0.01-1.0 MG/ML) antagonized not only the stimulatory effects of PGE but also the stimulatory effects of sodium fluoride and increased enzyme activity due to the previous treatment of cell cultures by cholera toxin. Both OPA and PPP produced a dose dependent depression of adenylate cyclase activity to zero values both under basal conditions and after stimulation by sodium fluoride and various hormones in all preparations studied, including rat liver, heart, brain, epididymal adipose tissue, small intestine, renal cortex and renal medulla. The present results indicate that both prostaglandin antagonists may, in higher concentrations, act as nonspecific inhibitors of the catalytic unit of adenylate cyclase rather than specific antagonists of the prostaglandin effects on adenylate cyclase.

Adenylyl Cyclases↗
PubMed1988

The effect of polyphloretin phosphate (PPP) on oral infiltration anaesthesia. An experimental investigation.

The possibilities to discontinue the anaesthetic effect using supplementary substances were studied. This investigation showed that administration of polyphloretin phosphate (PPP), 15 minutes after local anaesthetic injection, decreased the duration of infiltration anaesthesia of human teeth. The same result was also found when PPP was replaced by saline solution. However no effect on the duration of soft tissue anaesthesia was noted. There were no signs of adverse reactions.

Adult↗
PubMed1976

The cutaneous reactions to kallikrein, prostaglandin and thurfyl nicotinate in chronic urticaria and the effect of polyphloretin phosphate.

The erythema and wealing resulting from the application of thurfyl nicotinate ointment (Trafuril) and from the inoculation of kallikrein has been studied in patients with chronic urticaria and normal controls. Polyphloretin phosphate (PPP) suppressed the reaction in controls but in patients with urticaria it increased the reactions to Trafuril and had little effect on the kallikrein reaction. PPP also suppressed the PGE2-induced erythma in normal controls but not in urticaria patients. In a separate study using fibrinolysis autography, prostaglandin (PG) E2 and PGF2alpha depressed fibrinolysis in the skin of two pigs and both kallikrein and Trafuril suppressed fibrinolysis in human skin. It is suggested that the inflammatory reaction induced by thurfyl nicotinate and kallikrein is mediated in part by a prostaglandin-like action. Several anomalies in the action of Trafuril in skin diseases can be explained if such prostaglandin-like activity is mediated in part through inhibition of fibrinolysis.

Chronic Disease↗
PubMed1976

Polyphloretin phosphate reduces the algesic action of bradykinin by interfering with E-type prostaglandins.

(1) The method of the isolated perfused rabbit ear connected to the body by its nerve only was used to investigate the influence of the prostaglandin-antagonist polyphloretin phosphate (PPP) on the algesic effect of bradykinin (B) and acetylcholine (ACh). (2) Intra-arterial injections of B and ACh into the ear elicit a reflex fall in systemic blood pressure of the anaesthetized animal. PPP reduces this effects of B in proportion to the dose. The effect of ACh is reduced only to a small extent and only under higher concentrations of PPP than those necessary for inhibiting the effect of B. (3) Prostaglandin E1 (PGE1), when infused i.a. into the ear, enhances the effect of B and ACh by a sensitizing action on the perivascular pain receptors. PPP reduces or totally abolishes the PGE1-induced enhancement of the effect of B and ACh. (4) It is concluded that PPP reduces the effect of B mainly by inhibiting directly the pain enhancing action of the endogenously released PGs of the E-type. The effect of ACh is reduced only in the high concentration of PPP to a small extent probably by inhibiting the ACh-action rather than the sensitizing action of the only minimal released amounts of PGs. The PG-antagonizing action of PPP is further proven by the fact that during an additional infusion of PGE1 the enhanced effects of both B as well as ACh are reduced or abolished by PPP.

Acetylcholine↗
PubMed1983

Effect of polyphloretin phosphate on the contraceptive action of a polyethylene intrauterine device in rats.

A polyethylene intrauterine device (IUD) inserted in one horn of the rat uterus on Day 2 of pregnancy prevented implantation in 9 out of 12 rats in the horn with the device. When polyphloretin phosphate (PPP), a substance known to inhibit alkaline phosphatase, was administered to such rats from Day 1 till Day 5 of pregnancy, the device prevented implantation in only 3 out of 12 rats in the horn with the device. PPP also significantly reduced the raised levels of endometrial alkaline phosphatase observed in the presence of the device. A significant rise in endometrial alkaline phosphatase was seen in such animals not administered PPP. It is suggested that there is a correlation between the anti-implantation effect of an IUD and raised levels of endometrial alkaline phosphatase in rats.

Alkaline Phosphatase↗
PubMed1977

The effect of polyphloretin phosphate on the aqueous flare response to alpha-melanocyte stimulating hormone.

The breakdown of the blood aqueous barrier caused by topical prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) or subcutaneous alpha-melanocyte stimulating hormone (alpha-MSH) was quantified by measurements of the aqueous flare seen in the anterior chamber. Polyphloretin phosphate (PPP) administration subcutaneously was found to effectively block the protein leakage caused by all three traumatic stimuli. The same dose of PPP given intravenously inhibited effectively the flare response to PGE1 and alpha-MSH, whereas the effect of PGE2 was only slightly decreased. Significant inhibition by subconjunctival PPP was not achieved for any of the three stimuli. Assuming that PPP is a specific PG-antagonist the present results support the eariler suggestion that PGs take part in the barrier damaging action of alpha-MSH. However, it cannot be excluded that PPP acts on a step subsequent to PG. This step might be common to PGs- and alpha-MSH-effects on the barrier, explaining why PPP inhibits both types of trauma.

Administration, Topical↗