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PubMed1988

Evaluation of cytoprotective drugs for liver preservation by pyridine nucleotide fluorometry.

The cytoprotective effects of membrane-stabilizing drugs, such as chlorpromazine, allopurinol, dibucaine, phenoxybenzamine, and OP41483 (prostacyclin analogue), administered to perfusate and preservation medium were studied in rat liver, after 24 hours' preservation, by assessment of pyridine nucleotide fluorescence. On the fluorometric trace curve, amplitude (RxA) and velocity (RxV) from oxidation to reduction were determined. Percent decrease of RxA (%RxA) and that of RxV (%RxV) after 24 hours' preservation were calculated. At the end of preservation, the concentration of total adenine nucleotides of the liver, hepatic adenylate energy charge, and prepared mitochondrial oxidative phosphorylative activity were also measured. In the groups given phenoxybenzamine, dibucaine, and allopurinol, there was no significant difference among these parameters. In the chlorpromazine group, energy charge and %RxV were higher than in the drug-free group (p less than 0.05). In the OP41483 group, both energy charge and phosphorylation rate were significantly higher (p less than 0.05) and %RxV was significantly high (p less than 0.01) at concentrations of more than 3 nmol/L, compared with the values for those without drugs. These results suggest that the Redoximeter can provide accurate information on the effectiveness of cytoprotective drugs. It is also suggested that OP41483 has potential application for maintaining graft viability for human liver transplantation.

Allopurinol↗
PubMed1987

Gastric antisecretory and cytoprotective activity of MDL 646, a 16-methyl-16-methoxy prostaglandin E1 analog in man.

MDL 646 is a 16-methyl-16-methoxy PGE analog with gastric antisecretory and cytoprotective activity in rats following oral administration. The efficacy of MDL 646 in inhibiting pentagastrin-stimulated acid secretion in man was investigated in a pilot crossover study in 10 male subjects given single oral doses of 500-1,000 mcg of the compound or placebo in randomized order. The doses showing consistent antisecretory effects in all subjects were 800 and 1,000 mcg, which caused a reduction in acid output of at least 25% over the whole test period (2.5 h), with greater inhibition in the first hour. The cytoprotective activity of MDL 646 was investigated by measuring the ability of single oral doses of 500 mcg of compound to prevent the drop in gastric potential difference (PD) induced by aspirin. The study was carried out in 8 male subjects given MDL 646 or placebo in randomized order in accordance with a single-blind crossover design. MDL 646 prevented the aspirin-induced drop in PD: No adverse reactions or changes in bowel habits were reported in either study. The compound is worth investigating further as a potential anti-ulcer agent.

Administration, Oral↗
PubMed1986

Adaptive cytoprotection: an endoscopic study in man.

We studied the protective effect of the mild irritant 20% ethanol against the damage caused by the strong irritant 40% ethanol to the duodenal mucosa of 10 healthy volunteers. At time 0, placebo (1% ethanol) or 20% ethanol (6 ml) was sprayed directly onto the duodenal wall through an endoscope. After 15 min 40% ethanol (50 ml) was given; damage was assessed by endoscopic examination 30 min after ethanol. The damage was scored arbitrarily: score 0, no damage; 1, duodenal hyperemia; 2, one hemorrhagic lesion; 3, two to five hemorrhagic lesions; 4, five hemorrhagic lesions. In separate experiments, the effect of acetylsalicylic acid (20 mg/kg iv) on adaptive cytoprotection was evaluated. It was found that 1) 20% ethanol does not damage the duodenal mucosa, whereas 40% ethanol does; 2) duodenal hyperemia and hemorrhagic lesions caused by 40% ethanol can be prevented by the previous administration of 20% ethanol; and 3) acetylsalicylic acid does not damage the duodenal mucosa but abolishes the protective effect of 20% ethanol. "Adaptive cytoprotection" is a physiological phenomenon in humans too and further supports the probable defensive role of endogenous prostaglandins in the gastrointestinal tract.

Adolescent↗
PubMed1985

Cytoprotective effect of sofalcone in the rat gastric mucosa.

The effect of 2'-carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy)-chalcone (sofalcone, Solon) on 0.6N HCl-induced gastric lesions in the rat was studied. Sofalcone administered orally or intraperitoneally prevented the formation of gastric lesions induced by the necrotizing agent dose-dependently. Oral administration of sofalcone inhibited the aggravating effect of indometacin on the lesions induced by 0.6N HCl. Intraperitoneal administration of sofalcone also inhibited the aggravation of the lesions by indometacin treatment when it was given 30 min after the administration of sofalcone. This effect of sofalcone was not observed when indometacin was given 30 min before sofalcone. Simultaneous treatment with sofalcone and cimetidine inhibited the formation of the necrotic lesion synergistically. Carbenoxolone and cetraxate given orally protected the gastric mucosa against 0.6N HCl. Their protective effects were decreased when they were given intraperitoneally. These results suggested that the cytoprotective effect of sofalcone does not depend on the route of administration and that there are some interactions between cimetidine and sofalcone in their synergistic cytoprotective effects.

Administration, Oral↗
PubMed1985

Gastric cytoprotection by hyperosmotic solutions in the rat: role of endogenous prostaglandins.

Hyperosmotic solutions of xylitol exhibited significant antiulcer activity in the rat at osmotic concentrations (1000 mOs/1) which were devoid of antisecretory effect. The same solutions also protected the rat gastric mucosa against indomethacin and stress-induced erosions, and the protection was unaffected by the addition of 0.15 N HCl. Moreover, hyperosmotic solutions by xylitol, sorbitol or NaCl were protective against the necrotizing effect of NaOH (0.2 N) in a concentration-dependent manner. The cytoprotective action exerted by hyperosmotic solutions of xylitol against the NaOH-induced erosions was abolished, in a dose-dependent fashion, by pretreatment with the cyclooxygenase inhibitor indomethacin. It is concluded that in experimental ulcer models, in which the capacity of the mucosa to synthetize PG is unimpaired, the increased biosynthesis of prostaglandins resulting from exposure to hyperosmotic solutions may be crucial in the cytoprotective effect of the latter.

Animals↗
PubMed1984

Alternatives in hepatoprotection: cytoprotection--influences on mono-oxidase system--free radical scavengers (a review).

Three correlating fields of hepatoprotection have been reviewed: (1) "classic" gastrointestinal cytoprotection: (2) effects via the mixed function mono-oxidase enzyme system: (3) the role of the free radical scavengers and lipid peroxidation inhibiting agents. Gastrointestinal cytoprotection was originally defined in experimentally induced gastric mucosal injuries where several members of the prostaglandin group proved to be effective. Their capacity to increase the stability of biomembranes can be manifested also in hepatocytes, as PGE2 and PGI2 prevent the CCl4-toxicity in experimental animals. Induction of the mono-oxidase system (e.g. with barbiturates or with antioestrogens) may be useful by increasing bilirubin excretion and the biotransformation activity as well as possible by enhancing protein synthesis in liver cells. Inhibition of the mono-oxidases, on the other hand, can prevent the transformation of toxic substances into even more toxic metabolites and the production of free radicals. Free radical scavengers and inhibitors of lipid peroxidation play a central role in hepatoprotection. A flavonoid substance, (+)-cyanidanol-3 possessing many of the mentioned effects may be a promising alternative in the therapy of liver disease.

Animals↗
PubMed1983

Prostaglandins and gastrointestinal cytoprotection.

One of the important and interesting effects of prostaglandins in the gastrointestinal tract is cytoprotection: protection of the gastrointestinal mucosa against nonspecific injuries (physical, chemical, drugs, etc.). The characteristic features of cytoprotection, the possible mechanism of protection and the theoretical and clinical perspectives of prostaglandins and their analogues are discussed.

Animals↗
PubMed1983

Cytoprotection and 6-keto-prostaglandin-F1 alpha.

Several prostaglandins were found to protect the gastric mucosa against the ulcerogenic effect of immobilization (stress) and of indomethacin in the rat. The analogue 6-keto-prostaglandin-F1 alpha had no cytoprotective effect in the same region and even seemed to facilitate ulceration in the stomach in a dose-dependent manner. Unusually high doses of this prostaglandin analogue also exerted a slight cytoprotective effect.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Sulglycotide displays cytoprotective activity in rat gastric mucosa.

Sulglycotide, a well known antisecretory and antiulcer compound, has been further investigated for its ability to protect rat gastric mucosa against extensive necrosis induced by absolute ethanol, NaOH (0.2N) and NaCl (30%). Sulglycotide, which has been compared with cimetidine, displays a dose-dependent cytoprotective activity against the above necrotizing agents. The results obtained indicate that Sulglycotide requires a normal prostaglandin biosynthetic process in order to manifest its antiulcer activity. In fact gastric mucosa from animals treated with Sulglycotide releases in vitro a greater amount of PGl2-like activity; and furthermore no protection was observed against gastric lesions induced by indomethacin. As far as the mode of action of Sulglycotide is concerned it is tempting to speculate that the compound may interfere with prostaglandin degradation or it may trigger an adaptive cytoprotection which is important in maintaining the cellular integrity of rat gastric mucosa.

Animals↗
PubMed1984

A comparative dynamic study of the effectiveness of gastric cytoprotection by vitamin A, De-Nol, sucralfate and ulcer healing by pirenzepine in patients with chronic gastric ulcer (a multiclinical and randomized study).

The gastric cytoprotective effects of vitamin A, De-Nol and sucralfate were compared with the effectiveness of pirenzepine in healing ulcer in patients with chronic gastric ulcer. A total of 100 patients was randomized into different groups: the patients were treated with antacids, vitamin A (3 X 50.000 IU), De-Nol liquid (4 X 5 ml), sucralfate (4 X 1 g) or pirenzepine (3 X 50 mg). The treatment was continued for 4 weeks. At the beginning, 2 and 4 weeks after starting treatment the patients were subjected to endoscopy and the size of the ulcer was measured planimetrically. The ulcer-healing effect of De-Nol liquid was significantly better than that of the antacids (p less than 0.01). Ulcer size was reduced significantly in all groups (p less than 0.01), however, at the end of the study the gastric ulcers were smallest in the De-Nol treated group (p less than 0.001). The dynamics of ulcer healing in the second week was most favourable in the patients receiving vitamin A (p less than 0.01). The present data point to the cytoprotective effects of De-Nol liquid, vitamin A and sucralfate and to their ability of healing chronic gastric ulcers.

Adolescent↗
PubMed1984

Evidence for the existence of gastric cytoprotective effect of atropine and cimetidine in humans.

The effects of cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) were studied on the basal (BAO) and pentagastrin (6 micrograms X kg-1 s.c.)-stimulated (MAO) gastric acid secretion; the gastric mucosal microbleeding provoked by one-day treatment with indomethacin (4 X 25 mg orally) in patients with chronic disorders of the joints. The extent of the gastric microbleeding was measured by spectrophotometric determination of haemoglobin in gastric lavage fluid. The aims of this study were to determine the doses of cimetidine and atropine in humans without any significant inhibitory effects either on the basal or on the maximal gastric acid output to evaluate the cytoprotective action of these doses of cimetidine and atropine on the indomethacin-induced gastric microbleeding in the man. It was found that cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) did not cause any significant inhibition either of the BAO or of the MAO; indomethacin (4 X 25 mg orally) significantly increased gastric microbleeding in the patients; cimetidine and atropine, in the above doses, were able to prevent significantly indomethacin-induced gastric microbleeding in the patients. These results provide evidence for the existence of gastric cytoprotective effects of cimetidine and atropine in humans.

Adult↗
PubMed1984

In vitro and in vivo demonstration of the cytoprotective effect of (+)-cyanidanol-3.

In vitro and in vivo investigations were undertaken to demonstrate cytoprotective effect of (+)-cyanidanol-3 on human erythrocytes. The time of full haemolysis induced by hydrochloride acid was measured and dynamic haemolysis curve was recorded with an aggregometer. In vitro, following a one-hour incubation of erythrocytes with (+)-cyanidanol-3 at 37 degrees C, significant increase of the haemolysis time could be demonstrated. The most expressive cytoprotective effect was observed at (+)-cyanidanol-3 concentrations of 2, 5 and 10 micrograms/ml. In vivo, two hours following the oral administration of 1.5 g Catergen, an increase of the haemolysis time for about 25% could be demonstrated. This simple method seems to be suitable for the investigation of the membrane stabilizing effect of (+)-cyanidanol-3.

Benzopyrans↗
PubMed1984

Gastric cytoprotective properties of SCH 32651, a novel antiulcer agent.

The antisecretory activity of SCH 32651 (3-amino-2-methyl-8-phenylmethoxyimidazo[1,2-a] pyrazine HCl . 1/3 H2O) has been described in a preceding paper. This report describes its gastric cytoprotective properties. SCH 32651 inhibited the gastric lesions due to ethanol in a dose-dependent manner (ID50 = 5 mg/kg p.o.) and exerted its maximal effect when given 30 min before ethanol and had a duration of at least 90 min at 30 mg/kg p.o. The activity of SCH 32651 against ethanol was unaffected by indomethacin pretreatment. Furthermore, SCH 32651 produced significant increases in gastric mucus release (10-100 mg/kg p.o.) and rapidly reversed ethanol-induced (30-100 mg/kg p.o.) fall in gastric potential difference (PD). SCH 32651 displayed significant antiulcer activity in indomethacin-(30-100 mg/kg p.o.), aspirin - (30-100 mg/kg p.o.), "aspirin + acid" - (10-100 mg/kg p.o.), reserpine - (10-100 mg/kg p.o.), stress - (30-100 mg/kg p.o.), and cysteamine (10-100 mg/kg p.o.) ulcers. The present data in conjunction with those reported in a preceding paper indicate that SCH 32651 is an orally effective novel antiulcer drug with both gastric antisecretory and cytoprotective properties.

Administration, Oral↗
PubMed1984

Cytoprotective effect of prostaglandin E2 in irradiated rat ileum.

Radiation injury to the gastrointestinal tract is an infrequent but major clinical problem. Results of previous studies have shown that prostaglandins provide cytoprotection of the gastrointestinal mucosa against a variety of noxious agents, although, prior to this study, the protection against radiation exposure had not been documented. Exteriorized segment of Sprague-Dawley rat ileum was radiated with 10 and 15 Gy (137Cs). One group of rats was pretreated with prostaglandin E2 one hour before and 24 hours after radiation injury. The rats were sacrificed three and five days following radiation injury. Morphometric measurement of mucosal thickness, villous height, crypt of Lieberkühn height and number of mitosis per square millimeter swath of tissue were analyzed. Also, 125IUdR and 3HTdR were injected in a group of rats radiated with 15 Gy (137Cs). 125IUdR counts per minute per milligram of dry weight and 3HTdR labeled cells were counted and analyzed. The morphometric measurements and radioactive labeled tissue counts suggest that prostaglandin E2 has a cytoprotective effect upon irradiated rat ileum. Speculations about the possible mechanism and usefulness of this observation are included.

Animals↗
PubMed1983

Gastric cytoprotective effects of vitamin A and other carotenoids.

The effects of vitamin A and some carotenoids (beta-carotene, beta-cryptoxanthin, zeaxanthin, lutein, capsorubin, capsanthin, capsanthol and lycopene) were studied (a) on the development of acute gastric mucosal lesions produced by topical application of 0.6 M HCl and (b) on gastric secretion in 4-h pylorus-ligated rats. It was found (a) that vitamin A, beta-carotene, beta-cryptoxanthin, zeaxanthin and lutein significantly inhibited the development of gastric mucosal lesions produced by 0.6 M HCl, while capsorubin, capsanthin, capsanthol and lycopene failed to prevent the development of such lesions; and (b) that vitamin A, beta-carotene, beta-cryptoxanthin, zeaxanthin and lutein, i.e., the carotenoids which exerted a cytoprotective effect, had no inhibitory effect on gastric acid secretion in 4-h pylorus-ligated rats. The possible relationship between chemical structure and gastric cytoprotection is discussed.

Animals↗
PubMed1982

Gastric antisecretory, antiulcer and cytoprotective properties of 9-hydroxy-19,20-bis-nor-prostanoic acid in experimental animals.

9-Hydroxy-19,20-bis-nor-prostanoic acid (IBI-C83) was evaluated on gastric acid secretion and gastric lesions induced in laboratory animals by a variety of experimental conditions: compound IBI-C83 is proved effective in decreasing basal, histamine- and pentagastrin-stimulated total acid output in rats and in pentagastrin perfused dogs. The concentration of N-acetylneuraminic acid in the gastric fluid, a marker of mucus secretion, is enhanced in rats by IBI-C83. This drug prevents gastric damage induced by non-steroidal antiinflammatory compounds such as acetylsalicylic acid, indometacin and phenylbutazone, gastric ulcers following pylorus ligation, and facilitates healing of the gastric ulcers evoked by subserosal injection of acetic acid. A prominent feature of IBI-C83 is its capacity to protect the rat from gastric damage elicited by necrotizing agents such as absolute ethanol, hydrochloric acid and hypertonic saline. This property, called "cytoprotection" and common to naturally occuring prostaglandins, is independent on the antisecretory activity of IBI-C83 and is not shared, at least in the reported experimental models, by the H2-receptor antagonist cimetidine. In spite of the prostaglandin-like properties displayed in its cytoprotective activity, compound IBI-C83 does not affect cardiovascular functions, gastrointestinal transit and uterine motility.

Animals↗
PubMed1980

Experimental evidence for cytoprotective effect of atropine on the rat gastric mucosa.

The inhibitory effect of atropine on the gastric mucosal damage produced by topical aspirin has been studied in the rat, in the presence and in the absence of intragastrically applied 160 mmole/l HCl. The gastric mucosal damage was produced by aspirin given intragastrically in doses of 192 mg/kg. The topical application was done alone or in the presence of 160 mmole/l HCl. The ulcer incidence, the number and size of gastric mucosal damage were studied during 4 h. The aspirin solutions were administered with or without atropine (in doses of 4 and 10 mg/kg). The atropine was added immediately after the administration of aspirin. The results were as follows 1. A dose-dependent inhibition of ulcer incidence, number and size of gastric mucosal damage was produced by atropine in both groups of animals, when the aspirin was given alone or together with 160 mmole/l HCl; 2. The inhibitory effect of atropine was significantly weaker in the group treated with aspirin plus 160 mmole/l HCl than in th aspirin-treated group. It has been concluded the ulcer-preventing effect of atropine is mediated partly through the inhibition of gastric H+ secretion, and partly some "cytoprotective effect"; the extent of the "cytoprotective effect" of atropine was about half that on gastric H+ secretion.

Animals↗
PubMed1980

The role of mucus glycoproteins in prostaglandin cytoprotection.

The role of gastric mucus in the pathogenesis of septic erosions and as an explanation for prostaglandin cytoprotection is unclear. In a reproducible canine septic model bacterial peritonitis was induced in three groups of dogs. One group served as a control and each of the remaining groups received 16,16 dimethyl PGE2 either 0.2 microgram/kg. or 0.4 microgram/kg. I.M. q6h beginning 24 hours prior to peritonitis and continued during the septic period. Gastroscopy was performed and basal gastric juice collected prior to peritonitis and during the septic period. All animals in the control group developed acute gastric erosions and gastric juice protein significantly decreased while sialic acid and fucose significantly increased during the septic period. In the animals receiving 16,16 dimethyl PGE2 acute gastric erosions did not develop; sialic acid and fucose were significantly elevated compared to control dogs during sepsis. We conclude that prostaglandin cytoprotection may be related to increases in gastric glycoprotein secretion.

Animals↗