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At least 109 records · Page 6Linked to original sources
PubMed1991

[Effect of gastrin and enprostil, a PGE2 analog, on colonic cancerous cell growth].

The effects of gastrin (G-17), proglumide (a gastrin receptor antagonist), and enprostil (a synthetic analog of prostaglandin E2) used alone or in association were studied in colonic cancer Prob and Regb cell growth. The Prob (progressive in BD IX rats) and Regb (regressive) cell lines were cloned from a single chemically-induced rat colonic cancer. After a serum-free period corresponding to one doubling cell time, cells were incubated with 100 to 1,200 pM G-17, 40 or 80 mM proglumide, and 2.5 to 5 micrograms/ml enprostil for 8 h. Cell growth was measured 48 h later by colorimetric MTT assay. Two and four hundred pM G-17 gave a growth stimulation of 17.4 percent and 31 percent for Prob cells respectively or 35.5 percent and 49 percent for Regb cells. Growth stimulation was found to be statistically different (P less than 0.01) for Prob and Regb cells. Proglumide partially inhibited this growth stimulation whereas enprostil inhibited in totally. These results suggest that growth of some colonic cancer cell lines may be G-17 dependent. However the intensity of cell-growth stimulation depends on the level of cell malignancy or differentiation in a single tumor.

Adenocarcinoma↗
PubMed1986

[Stomach ulcer healing with enprostil, an orally effective prostaglandin E2 analog: direct comparative study with ranitidine].

In a randomized, endoscopically controlled double-blind trial the effectiveness of a twice daily dose of the prostaglandin E2-analogue enprostil was compared with ranitidine given to 93 ambulatory patients with benign gastric ulcers. Under 35 micrograms b.i.d. enprostil the ulcer healing rates after 2, 4, 6 and 8 weeks averaged 22% (10/46), 58% (26/45), 80% (35/44) and 86% (37/43). The corresponding values for ranitidine 150 mg b.i.d. were 22% (10/46), 66% (29/44), 84% (38/45) and 89% (41/46). The differences were not statistically significant. Both drugs had a similar influence on the ulcer symptoms and were well tolerated. The findings suggest that enprostil can be given in a twice daily dosage in the treatment of benign gastric ulcers.

Clinical Trials as Topic↗
PubMed1993

Effects of PGE2, misoprostol, and enprostil on guinea pig enterocyte adenylate cyclase. Clinical implications.

Prostaglandins of the E series (PGE) are known to stimulate intestinal water and electrolyte secretions via the activation of the enterocyte adenylate cyclase. Their methylated synthetic analogs misoprostol and enprostil induced diarrhea in 5-13% of the patients in most clinical studies. In order to elucidate the role of PGE-adenylate cyclase interaction in these phenomena, we studied the stimulation of adenylate cyclase by native prostaglandin E2 (PGE2) and synthetic PGE analogs on isolated guinea pig intestinal epithelial cells. PGE2 stimulation of adenylate cyclase was dose-dependent, reaching a maximum for 3 x 10(-4) M, with an EC50 of 3.7 x 10(-6) M. The Hill analysis of the concentration-response curve gave a straight line, with a slope close to 1. The effect of PGE2 was strictly additive to that of 10(-5) M forskolin, whereas it was decreased in terms of potency by 10(-9) M cholera toxin. Somatostatin-14 markedly inhibited PGE2 stimulation by 37% and 45% with 10(-9) M and 10(-6) M, respectively. The two PGE methylated analogs misoprostol and enprostil were less potent than PGE2 in stimulating adenylate cyclase in our model.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1995

A comparison of two prostaglandin analogues (enprostil vs misoprostol) in the treatment of acute duodenal ulcer disease.

We conducted a clinical trial to compare the efficacy and safety profile of two prostaglandin analogues, enprostil (35 micrograms twice daily) and misoprostol (200 micrograms four times daily) in the treatment of acute duodenal ulcers in 214 patients. The two agents healed approximately 80% and in excess of 90% of duodenal ulcers after 4 and 6 weeks' therapy, respectively. There was a significantly lower ulcer healing rate in both treatment groups in smokers compared with non-smokers (P < 0.05). However, daytime and nighttime ulcer pain relief was achieved in fewer than 50% of patients by either agent. Diarrhea, which occurred in more than 40% of patients, was the predominant side effect, and occurred mainly during the first 2 weeks of therapy with either agent. Nevertheless, this side effect was mild and self-limiting in the majority of patients. Both agents were found to be safe and well tolerated by the majority of patients. We conclude that these prostaglandin analogues are safe and effective duodenal ulcer healing agents. Furthermore, there was very little difference between enprostil and misoprostol. The limiting factors, however, for their routine use as ulcer healing agents are their low efficacy with regard to ulcer pain relief and the high incidence of diarrhea.

Acute Disease↗
PubMed1986

Gastric mucosal binding studies with enprostil: a potent anti-ulcer prostaglandin.

The potent antiulcer prostaglandin enprostil binds with high affinity to porcine gastric mucosal tissues. This binding is saturable, dissociable and displaceable by compounds with similar structures. Various characteristics of binding such as pH optimum and displacement potencies suggest that enprostil binds to mucosal PGE2 sites. Structure-activity and gastric mucosal binding relationships were also examined.

Animals↗
PubMed1988

Enprostil inhibits post-prandial gastrin release: a dose-response study.

In a double-blind placebo-controlled study in nine healthy volunteers, the effects of single doses of oral enprostil (8.75, 17.5, 35 and 70 micrograms), taken before a standard breakfast, were assessed on the post-prandial release of gastrin into the plasma. All doses of enprostil caused a significant dose-related decrease in median post-prandial plasma gastrin concentration (range from -29 to -44%). In the same subjects, two doses of 25 mg indomethacin caused a significant (38%) increase in median post-prandial plasma gastrin concentration.

Adult↗
PubMed1986

Effect of enprostil, a synthetic prostaglandin E2 on 24 hour intragastric acidity, nocturnal acid and pepsin secretion.

We have studied the effect of a prostaglandin E2 analogue (enprostil), on intragastric acidity, gastric acid and pepsin outputs during a 24 hour period in nine patients with duodenal ulcer in remission. Enprostil 35 micrograms bd dose inhibited 24 hour intragastric acidity by 38% and a 70 micrograms nocturnal dose by 33%. Decrease in nocturnal pepsin secretion was both volume and concentration related.

Adult↗
PubMed1986

[Enprostil in the acute treatment of duodenal ulcer: direct comparative study with pirenzepin].

In a randomized, endoscopically controlled double-blind trial the effectiveness of a twice daily dose of the prostaglandin E2-analogue enprostil was compared with pirenzepine given to 97 ambulatory patients with duodenal ulcers. Under 35 micrograms b.i.d. enprostil the ulcer healing rates after 2, 4 and 6 weeks averaged 41%, 82% and 92%. The corresponding values for pirenzepine were 44%, 72% and 89%. The differences were not statistically significant. Both drugs had a similar influence on the ulcer symptoms.

Acute Disease↗
PubMed1994

[Sensitivity of gastric parietal cells to histamine after administration of enprostil and ranitidine during 4 weeks in healthy subjects].

Parietal cell sensitivity is increased in patients with active duodenal ulcer. It has been shown to increase in healthy volunteers after a 4-week treatment with H2-receptor blockers. Metaanalyses of therapeutic trials have indicated that time to first relapse was longer after ulcer healing with prostaglandins (PG) than after healing with H2-receptor blockers, which might be due to a different effect of the two treatments on parietal cell sensitivity. OBJECTIVES--To study, in healthy volunteers, basal gastric acid secretion, acid secretory responses and parietal cell sensitivity to histamine before and after a 4-week treatment with enprostil (E) and ranitidine (R). METHODS--This was a randomized double-blind double-dummy crossover study. Twelve male healthy volunteers (22-44 years) were randomly assigned to receive a 4-week treatment with either E (35 micrograms bid) or R (150 mg bid). After a 2-month washout period, they were crossed to the alternate treatment. Basal acid output (BAO), acid secretory responses to low-dose histamine infusion (histamine dihydrochloride 2.5 micrograms/kg/h) (LDAO), to a high-dose histamine infusion (25 micrograms/kg/h) (HDAO) and parietal cell sensitivity (PCS = LDAO/HDAO x 100) were measured 24 hours before the first administration and 72 hours after the last administration of each medication. RESULTS--All secretory parameters were similar before treatment with E and R. As compared to pretreatment values: a) HDAO tended to increase after both treatments (NS); b) LDAO (m +/- sem) slightly increased after R (18.4 +/- 2.6 vs 13.9 +/- 3.3 mEq) (NS) but not after E (12.5 +/- 1.8 vs 13.2 +/- 1.9 mEq); c) PCS (m +/- sem) was unchanged after R (36 +/- 4 vs 33 +/- 6) but decreased after R (30 +/- 6 vs 36 +/- 0.5; P < 0.02). When secretory parameters after treatment with R and treatment with E were compared, the difference was significant for LDAO (P < 0.02) and PCS (P < 0.05). CONCLUSIONS--If also found in patients with duodenal ulcer disease, these results might, at least partly, explain the lesser propensity of the ulcers to relapse early after healing with PG than after healing with H2-receptor blockers. However enprostil has been with-drawn from the market and it is now well established that one factor influencing the relapse rate is the efficiency of the treatment given to achieve ulcer healing in eradicating Helicobacter pylori. Consequently, the interest of our results is presently mostly physiological.

Adult↗
PubMed1991

Determination of femtomole/milliliter concentrations of enprostil acid in human plasma using high-performance liquid chromatography-laser-induced fluorescence detection.

This paper describes the use of multiple-column high-performance liquid chromatography (HPLC) combined with laser-induced fluorescence for the determination of femtomole/milliliter concentrations of enprostil acid, a prostaglandin analogue, in human plasma. The drug is isolated from plasma by phenyl solid-phase extraction and fluorescently labeled at its carboxyl functional group with a large excess of 2-bromoacetyl-6-methoxynaphthalene. A multi-column method using both normal- and reversed-phase chromatography is necessary to separate the labeled drug from the unreacted reagent. Post-column dilution of the mobile phase with water after the reversed-phase chromatography allows on-line concentration of the labeled analyte onto a guard column prior to the microbore HPLC. A loop guard column device provides a simple way to inject up to 1.0 ml of sample solution onto a microbore column without significantly reducing the column efficiency. A 325-nm He-Cd laser is used to excite the labeled drug, and fluorescence emission is monitored at 450 nm. Using this system, we are able to derivatize, detect, and quantify 5 pg of the prostaglandin analogue in 1.0 ml of plasma.

Chromatography, High Pressure Liquid↗
PubMed1986

Platelet function in patients receiving enprostil.

The effect of 14 days of treatment with enprostil (35 micrograms twice daily) or ranitidine (150 mg twice daily) on platelet function in 21 patients with duodenal ulcer was evaluated in a double-bind, randomized, parallel study. Platelet function, as determined by the results of a coagulation screen, aggregation tests, and an assay for plasma beta-thromboglobulin levels, was assessed before and after 14 days of treatment. No effect on platelet function was observed with either drug in this group of patients.

Adult↗
PubMed1992

Effects of the prostaglandin E2 analogue enprostil on the carbon tetrachloride-induced necrosis of liver cells in mice.

Female mice, eight weeks old, were injected with carbon tetrachloride (CCl4) (10 mg subcutaneously). Groups of mice (n = 10-30) were then injected with enprostil (E) 2, 20 or 50 micrograms/kg body weight (bw) intraperitoneally 15 min and two h after, or E 100 micrograms/kg bw two h after the CCl4 injection. The mice were killed after 24, 48 or 72 h. Plasma activity concentrations of alanine aminotransferase (ALAT) were determined in blood specimens from the iliac veins. The extent of liver cell necrosis in histological sections was recorded on a 100 mm Visual Analogue Scale (VAS) and measured using the electronic Mini Mop method. In the group given the highest single dose of E (100 micrograms/kg) a significant lowering of the CCl4-induced liver cell necrosis was found after 24 h. No significant differences were found after 48 and 72 h. In the other groups injected with lower doses of E after CCl4, no significant differences were found compared to groups injected with CCl4 alone.

Alanine Transaminase↗
PubMed1987

[Effects of enprostil on changes in the gastric transepithelial potential differential induced by aspirin].

Enprostil (E), is a semisynthetic E2 prostaglandin with wide-range antisecretory properties. Administered orally E reduced mucosal injury in rats exposed to NSAID and gastric acid. The aim of the present study was to analyze the cytoprotective effect of 7 micrograms of E on the aspirin-induced (500 mg) decrease in gastric transepithelial difference of potential (DP) in a) five healthy volunteers and b) five patients with epigastric heartburn, normal endoscopy and a low gastric DP (mucosal barrier weakness). Aspirin-induced decrease of gastric DP was measured during two four hour periods separated by an interval of two days: a) during a one hour basal period and after three hours after 7 micrograms of E, and b) during a second basal period and one hour after aspirin, E, and then aspirin again. The following parameters were analyzed: maximal drop of DP DP Max (mV), area under the curve of DP drop, AUC (mV.min), and time to return to basal values, TRB (min). In the control group, when E was administered after aspirin, the decrease in DP Max (11.4 +/- 2.3 vs 6.6 +/- 2.1) and in AUC (68 +/- 22 vs 35 +/- 11) was significant (p less than 0.05) as compared with values obtained after aspirin alone. In the patient group, E produced a significant decrease in aspirin-induced DP Max (11.8 +/- 1.9 vs 6.8 +/- 2.4) (p less than 0.003) and in AUC (117 +/- vs 48 less than 22) (p less than 0.006) as well as in TRB (52 +/- 2 vs 37 +/- 10) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗