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PubMed1990

[Observing cytoprotection of indomethacin on primary cultured hepatocytes of rats].

We observed previously that indomethacin induced hepatic protection against CCl4 and galactosamine in rats. In this work we further investigated this phenomenon on primary cultured rat hepatocytes. The results showed that cultured hepatocytes of rats pretreated with indomethacin in vivo still retained the ability resisting CCl4-induced cytotoxicity, as indicated by lower leakage of enzymes. However, cultured hepatocytes of normal rats treated with indomethacin in vitro had no obvious resistance to CCl4-induced cytotoxicity. The results suggest that indomethacin pretreatment in vivo enables hepatocytes to resist injury, which probably also needs participation of other factors.

Animals↗
PubMed1989

[The cytoprotective effect of prostaglandin E2 in duodenal ulcers].

Intragastric administration of a synthetic analog of prostaglandin E2 to patients with duodenal ulcers results in depression of the gastric acid production and in reduction of potassium level, leads to an elevation of the sialic acid debit and a rise of sodium concentration, not essentially changing calcium, chlorides, and pepsin levels. A combined analysis of gastric acid production and measurements of sialic acids, sodium and potassium detect the imbalance of the mucoid and bicarbonate secretion in peptic ulcers, this helping predict the disease course.

Adolescent↗
PubMed1989

Effect of cytoprotective and antiulcer drugs on the healing process of subacute gastric ulcer in rat (a new model).

It has been developed by us a simple new method for producing subacute gastric ulcer in rats, combined with a novel method for the quantitative evaluation of the healing process. Fasted rats with 120-150 g were used. The animals were anaesthesized by ether and than a polyethylene chateter was orally inserted into the stomach with a fine needle inside. After the cannule reached the gastric wall, the needle was pressed gently so as to punch the gastric wall. Drugs under study were administered orally 30 min and 24 h after the puncture. Food and water were given ad libitum from 2 h after the intervention until the end (96 h) of experiments. In order to follow the healing process of subacute ulcer, the so-called tensile strength of the ulcer was determined by inflating and expressed in mmHg. The healing rate was calculated. The antiulcer drugs: Cimetidine, Famotidin, Pirenzepine and sucralfate dose dependently and significantly increased the healing rate of ulcer. Non steroidal antiinflammatory drugs: naproxen, piroxicam, indomethacin and ibuprofen significantly delayed the healing of ulcer. ASA showed tendency to delay the healing. Strong HCl (0.5 molar) significantly delayed the healing of ulcer. N-EM given subcutaneously dose dependently delayed the healing of subacute ulcer.

Animals↗