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Biomedical subjects

J Puurunen

Publications and source records attributed to J Puurunen.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effect of ethanol on peptic activity in the rat stomach.

The action of ethanol on peptic activity in the stomach was evaluated by studying ethanol-induced changes in pepsinogen secretion in the rat in vivo and the effects of ethanol on pepsinogen and pepsin in vitro. Irrigation of the stomach with 3% ethanol in 100 mM HCl plus 50 mM NaCl had no effect on pepsinogen secretion, whereas 10 and 20% ethanol gave maximal increases of about 40 and 65%, respectively. 10% ethanol in 150 mM NaCl (pH 5.0) stimulated pepsinogen secretion maximally by about 60%. 10% ethanol in distilled water had no effect on spontaneous secretion of pepsinogen, but enhanced pepsinogen secretion induced by irrigation of the stomach with 100 mM HCl, 100 mM NaCl, 150 mM sucrose, or by an intravenous injection of carbachol. Ethanol inhibited the activation of pepsinogen to pepsin in vitro in a pH-dependent manner. The activity of pepsin was inhibited by ethanol with an IC50 value of about 10%. The results indicate that the effects of ethanol on pepsinogen secretion and the enzymes, pepsinogen and pepsin, are opposite in the rat. It is thus difficult to conclude what are the net effects of various concentrations of ethanol on the peptic activity of the gastric content, but at least higher concentrations can be expected to reduce this activity.

Animals↗
PubMed1980

Gastric mucosal blood flow in ethanol-induced mucosal damage in the rat.

Gastric mucosal blood flow in ethanol-induced mucosal damage was studied in urethane-anaesthetic rats by reference to 14C-aminopyrine clearance in the gastric mucosa. Irrigation of the stomach with 30% ethanol in acid saline (100 mM HCl plus 50 mM NaCl) for 40 min broke the gastric mucosal barrier, as indicated by an increased outflow of Na+ and K+ ions and back-diffusion of H+ ions. Gastric mucosal blood flow also increased about 2-fold decreasing after cessation of ethanol irrigation along with the net ion fluxes. The increase in gastric mucosal blood flow occasioned by 10, 20 and 30% ethanol in acid saline was directly proportional to the net fluxes of H+, Na+ and K+ ions. When the stomach was irrigated with 30% ethanol in a less acid medium (10 mM HCl, 90 mM choline chloride plus 50 mM NaCl) there was still a significant increase in the outflow of Na+ and K+ ions, but only a slight-back-diffusion of H+ ions. During this low rate of acid back-diffusion 30% ethanol reduced gastric mucosal blood flow by about 50%. The results suggest that ethanol-induced mucosal damage in the rat is associated with an increase in gastric mucosal blood flow only if combined with back-diffusion of H+ ions.

Animals↗
PubMed1980

Effect of cimetidine on microsomal drug metabolism in man.

The effect of cimetidine on human microsomal drug metabolism was studied. In five of six healthy volunteers therapeutic doses of cimetidine prolonged the half-life of antipyrine (range 12-37%; p < 0.05). Its clearance was decreased in five subjects (range 2-18%) and was increased in one subject (15%), the changes not being statistically significant. The volume of distribution increased on average by about 14% (range 9--19%; p < 0.001). Cimetidine in vitro inhibited the hydroxylation of benzo(a)pyrene and coumarin, as well as the O-deethylation of 7-ethoxycoumarin, by homogenised liver biopsies. The in vitro studies suggest that the effect of cimetidine on antipyrine elimination is due to inhibition of microsomal drug metabolism, which may prove an important drug interaction.

Adult↗
PubMed1980

Is ethanol-induced damage of the gastric mucosa a hyperosmotic effect? Comparative studies on the effects of ethanol, some other hyperosmotic solutions and acetylsalicylic acid on rat gastric mucosa.

The involvement of hyperosmolarity in ethanol-induced gastric mucosal damage was studied by comparing the effects of ethanol on the rat gastric mucosa and those caused by hyperosmotic glucose and choline chloride solutions, and by an almost isosmotic solution of acetylsalicylic acid. Upon intragastric instillation, all test solutions, namely 3M and 5M ethanol (3330 and 5590 mosmol/kg resp.), 3M glucose (3890 mosmol/kg), 1.5 M choline chloride (2840 mosmol/kg) and 20 mM acetylsalicylic acid, also containing 100 mM HCl and 50 mM NaCl, produced macroscopic and microscopic lesions of the gastric mucosa. The haemorrhages induced by ethanol and acetylsalicylic acid solutions were more evenly distributed, whereas most lesions produced by the glucose and choline chloride solutions were located at the rumeno-fundic junction. There were no qualitative differences between the microscopic lesions caused by the various instillates, however. All the test solutions broke the gastric mucosal barrier and increased histamine release and pepsinogen output, but in the rats treated with acetylsalicylic acid these effects were less pronounced. Ethanol, glucose and choline chloride solutions increased gastric mucosal flow and fluid output from the stomach, whereas acetylsalicylic acid had no effect on these. The similarity between the ethanol-induced changes and those caused by hyperosmotic solutions of glucose and choline chloride leads to the suggestion that ethanol may cause damage in the gastric mucosa at least in part, via hyperosmolarity.

Animals↗
PubMed1980

Effect of prostaglandin E2, cimetidine, and atropine on ethanol-induced gastric mucosal damage in the rat.

The effect of prostaglandin E2 (PGE2), cimetidine, and atropine on ethanol-induced gastric mucosal damage was studied in anaesthetised rats. Intravenous infusion of PGE2 (120 micrograms/kg X h) protected the gastric mucosa against lesions produced by irrigation of the stomach with 30% (v/v) ethanol in 100 mM HCl plus 50 mM NaCl. PGE2 had no effect on back-diffusion of H+ ions, whereas outflow of Na+ and K+ ions decreased. The increases in pepsinogen secretion and gastric mucosal blood flow during mucosal damage were not affected by PGE2. Cimetidine (25 mg/kg intravenously) failed to prevent mucosal haemorrhages induced by ethanol. Cimetidine caused a slight decrease in outflow of Na+ ions but otherwise had no effect on the variables measured. Atropine sulphate (1 mg/kg X h intravenously) similarly did not protect the gastric mucosa against ethanol-induced lesions, nor did it change ion fluxes, fluid output, or pepsinogen secretion during mucosal damage. Gastric mucosal blood flow, however, was lower in the atropine-treated rats than in the control rats. The results indicate that PGE2, but not cimetidine or atropine, protects the gastric mucosa against ethanol-induced damage in anaesthetised rats, but that this effect is not due to prevention of back-diffusion of H+ ions or to increased mucosal blood flow.

Animals↗
PubMed1979

Effect of intragastric acid on pepsinogen secretion in the rat.

When the osmolarity of intragastric instillates was constant (200 mosmole/l) the changes in their hydrogen ion concentrations (maximally from 0.01 to 100 mM) did not significantly affect pepsinogen secretion in anaesthetised rats. Solutions of 100 mM HCl, 100 mM NaCl and 150 mM sucrose all produced a similar stimulation of pepsinogen secretion. The results do not support the view that the gastric mucosa contains receptors sensitive to hydrogen ions regulating pepsinogen secretion under physiological conditions.

Animals↗
PubMed1978

Osmotic stimulation of pepsin secretion in the rat.

The effect of the osmolarity of intragastric instillates on pepsin secretion was studied in rats anaesthetised with urethane. Irrigation of the stomach with solutions of sucrose and NaCl, resp. caused a concentration-dependent increase in pepsin output. A stimulation was observed already by hypotonic solutions and the maximal effect was obtained by 300 m-osmole/l of sucrose and by 600 m-osmole/l of NaCl (13- and 10-fold stimulation resp.). A similar time course in the increase of pepsin output was produced by hyperosmotic solutions (600 m-osmole/l) of sucrose, urea, NaCl and choline chloride. Pepsin output was stimulated maximally within 30 min and decreased thereafter, but remained at about 4--6-fold higher levels than during the previous irrigation with distilled water. Replacement of hyperosmotic instillates by distilled water reduced pepsin secretion to the initial level. Hypertonic ethanol (600 m-osmole/l) increased pepsin output only slightly. Vagotomy, pretreatment with atropine (1 mg/kg i.v.) or cimetidine (5 mg/kg i.v.), local anesthesia of the gastric mucosa with 4% lidocaine or intravenous infusion of PGE2 (2 microgram/kg X min) did not antagonise the stimulation of pepsin output induced by hyperosmotic NaCl (600 m-osmole/l). The results indicate that the increase of the osmolarity of intragastric instillates stimulates pepsin secretion in the rat without involvement of neural (vagal or local cholinergic reflexes) or hormonal mechanisms (release of gastrin) which are known to stimulate gastric secretion in the gastric phase.

Animals↗
PubMed1977

Ethanol-induced changes in gastric mucosal content of cyclic AMP and ATP in the rat.

The stomach of urethane-anaesthetised rats was perfused with 10% (v/v) ethanol. At 40 min, the secretion of acid was strongly inhibited and the contents of cyclic AMP and ATP were lowered in the superficial mucosa, but not in whole gastric mucosa. After discontinuation of the ethanol perfusion, the rate of gastric acid output as well as the cyclic AMP and ATP levels recovered. Most of the acid-secreting parietal cells were found in the superficial mucosa where the changes of cyclic AMP and ATP took place. The results suggest that lowering of the mucosal contents of cyclic AMP and ATP may be involved in the ethanol-induced inhibition of the gastric acid output.

Adenosine Triphosphate↗
PubMed1976

Ethanol, indomethacin and gastric acid secretion in the rat.

In the anesthetized rat, 10% ethanol in the gastric lumen causes a total cessation of the secretion of gastric acid within 30--60 min. This effect is inhibited by pretreatment with indomethacin, which is a potent inhibitor of prostaglandin synthesis. Therefore, the inhibitory effect of local ethanol on gastric acid secretion in the rat may be mediated, at least partly, by increased synthesis of prostaglandins.

Animals↗
PubMed1976

Effects of ethanol on the cyclic AMP system of the dog gastric mucosa.

The effect of ethanol on the cyclic AMP system of the dog fundic mucosa was studied in vitro. The gastric mucosal content of cyclic AMP was increased by 2.5% ethanol, whereas 10 and 20% ethanol decreased the mucosal content of cyclic AMP. The activity of adenylate cyclase was increased by 2.5 and 5% ethanol, whereas 10% ethanol did not significantly affect it. The activity of cyclic AMP phosphodiesterase was inhibited by ethanol in a competitive manner. The increase in the gastric mucosal content of cyclic AMP, induced by low concentrations of ethanol, is apparently due to the stimulation of adenylate cyclase and inhibition of phosphodiesterase. Changes in the phosphodiesterase or adenylate cyclase activites do not explain the decrease of the mucosal content of cyclic AMP by higher concentrations of ethanol. The mechanism of the decrease is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1976

Effects of ethyl alcohol on the adenosine 3', 5'-monophosphate system of the human gastric mucosa.

The effect of ethyl alcohol on the cyclic AMP system of the human gastric mucosa was studied in vitro. Corporic gastric mucosa was obtained from patients operated on for gastric or duodenal ulcers. Under the in vitro conditions used, ethanol at concentrations of 5% (v/v) or less stimulated the activity of adenylate cyclase and induced a dose-dependent rise of the gastric mucosal content of cyclic AMP. However, 10% ethanol increased the activity of adenylate cyclase but did not affect the gastric mucosal content of cyclic AMP. At the concentrations of 5 or 10%, ethanol inhibited the activity of cyclic AMP phosphodiesterase in a competitive manner. Reports in the literature indicate that oral ethanol stimulates the output of gastric acid at low but not at higher concentrations. The present results are consistent with the conception that the stimulatory effect of ethanol on the output of acid is mediated by an increase of the content of cyclic AMP in the gastric mucosa.

Adenylyl Cyclases↗