PubMed Health⌕ Search

Biomedical subjects

J Garlicki

Publications and source records attributed to J Garlicki.

14 recordsLinked to original sources
PubMed1998

[Glutamine--its metabolic role and possibilities for clinical use].

Glutamine has been the point of interest of many nutritional studies concerning parenteral and enteral nutrition. Advantages from glutamine support have been observed previously in animal models. It was shown that glutamine is the energy source for rapidly dividing cells e.g. immune cells, gut mucosa. Recent molecular and protein chemistry studies have begun to define metabolic mechanism of glutamine action, and clinical trials suggest its safe and positive influence on catabolic patients. Parenteral and enteral nutrition enriched with glutamine improves gut integrity and function, decreases infection rate and improves function of immune cells. However, the indications for glutamine enriched nutrition and appropriate protocol of administration need determination. Taken together the data suggest that this amino-acid is an important dietary nutrient and is probably conditionally essential in certain catabolic conditions.

Animals↗
PubMed1991

Role of acid milieu in the gastroprotective and ulcer-healing activity of sucralfate.

Sucralfate prevents the formation of acute gastric lesions induced by various ulcerogens and enhances the healing of chronic gastroduodenal ulcerations, but the mechanism of these effects has not been fully explained. This study was designed to determine the importance of intragastric pH in the sucralfate-induced gastroprotection against 100% ethanol, acidified aspirin, taurocholate, or stress, and in the healing of chronic gastroduodenal ulcerations induced by acetic acid. Sucralfate acidified to pH 2.0 showed significantly stronger protective activity against all four irritants, its protective potency against 100% ethanol being about eight times greater and the duration of the protection about four times longer than those obtained with sucralfate at its pH of 5.0. Pretreatment with indomethacin to suppress mucosal generation of prostaglandin or the removal of salivary glands to eliminate the endogenous source of epidermal growth factor failed to affect sucralfate-induced gastroprotection. In contrast, the rate of healing of chronic gastric ulcerations was significantly delayed by indomethacin or sialoadenectomy; but sucralfate enhanced the healing, and a marked inhibition of gastric acid secretion by ranitidine did not eliminate this enhancement. We conclude that the protective activity of sucralfate depends on the presence of acid milieu in the stomach, but that the ulcer-healing effects of this drug occur even after a marked inhibition of gastric acid secretion.

Animals↗
PubMed1991

Nocloprost, a unique prostaglandin E2 analog with local gastroprotective and ulcer-healing activity.

Nocloprost (9 beta-chloro-16,16-dimethyl prostaglandin E2 (PGE2)) was examined for gastroprotective and ulcer-healing activity and compared to 16,16-dimethyl PGE2 (dmPGE) in rats. Nocloprost given intragastrically (i.g.) at various doses (0.01-10 micrograms/kg) 30 min before 100% ethanol, acidified aspirin (ASA), acidified taurocholate, water immersion, or restraint stress dose dependently prevented the formation of gastric lesions, the ID50 values being 0.25, 0.58, 0.06 and 0.12 micrograms/kg, respectively. The gastroprotection provided by nocloprost given i.g. was somewhat enhanced by the presence of acid in the stomach and was reduced by inhibition of gastric acid secretion. Nocloprost given s.c. also showed protective activity against ethanol damage but was ineffective when applied intraduodenally. The protective effect of nocloprost lasted about 8 h whereas that induced by dmPGE lasted 6 h. Nocloprost (0.01-100 micrograms/kg) given i.g. failed to affect gastric acid secretion or intestinal secretion (enteropooling) but prevented the increased gastroduodenal alkaline secretion. Nocloprost alone caused only a transient increase in the mucosal blood flow but prevented the fall in blood flow caused by 100% ethanol. [3H]Nocloprost was absorbed from the small intestine but was then taken up and metabolized by the liver and excreted into the bile so that very little reached the systemic circulation in an unchanged form. Nocloprost, unlike dmPGE, accelerated the healing of chronic gastric ulcerations and enhanced mucosal growth. We conclude that nocloprost is a locally active PGE2 analog with high cytoprotective and ulcer-healing efficacy.

Animals↗
PubMed1991

Role of polyamines and prostaglandins in gastroprotective action of epidermal growth factor against ethanol injury.

Epidermal growth factor (EGF) exhibits its gastroprotective action against a variety of irritants and ulcerogens and plays an important role in healing of acute and chronic gastroduodenal ulcerations, but the mechanisms of these effects are not known. The present study was undertaken to determine whether polyamines (such as spermine or putrescine) and prostaglandins (PGs), which also show protective properties, contribute to the gastroprotective effect of EGF against ethanol injury in rats. It was found that both EGF and polyamines significantly and dose-dependently prevented the formation of gastric lesions induced by absolute ethanol, the effect being similar to that obtained with 16,16-dimethylprostaglandin E2. Pretreatment with indomethacin failed to affect the gastroprotective action of EGF and polyamines, suggesting that endogenous PGs may not play any major role in this protection. Our finding that the protective effect of EGF can be abolished by pretreatment with DFMO, an inhibitor of the polyamine biosynthetic pathway, suggests that gastroprotection by EGF is due, at least in part, to stimulation of biosynthesis of protective polyamines.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Intragastric pH in the gastroprotective and ulcer-healing activity of aluminum-containing antacids.

Antacids containing aluminum have been shown to stimulate the protective processes in the gastric mucosa and to enhance the healing of chronic gastroduodenal ulcerations, but the mechanisms of these effects are still unexplained. This study was designed to compare the protective effects of unmodified and acidified (pH 2.0) Maalox 70 and Al(OH)3 on the formation of acute gastric mucosal lesions induced by absolute ethanol, taurocholate, acidified aspirin and stress, and to determine the role of gastric acid in healing of chronic gastroduodenal ulcerations by these antacids in rats. Acidified Maalox 70 and Al(OH)3 were significantly more potent than unmodified agents against all four tested types of acute mucosal lesions, and this action was probably due to their 'mild irritant' effect as evidenced by extensive exfoliation of the surface epithelial cells observed microscopically after the exposure of the mucosa to these agents. Mucosal generation of prostaglandins does not appear to be involved in the gastroprotection by acidified Maalox because the pretreatment with indomethacin did not affect this protection. In contrast to the protective effect, the ulcer-healing capacity of Maalox or Al(OH)3 does not appear to be dependent upon the presence of gastric acid because the reduction or elimination of endogenous acid by the pretreatment with ranitidine or omeprazole did not affect the healing of gastroduodenal ulcerations. We conclude that aluminum-containing antacids induce the mucosal protection that is enhanced in the presence of luminal acid but exhibit an ulcer-healing property that appears to be unrelated to gastric acid secretion or mucosal generation of prostaglandins.

Acute Disease↗
PubMed1990

Cholecystokinin receptors and vagal nerves in control of food intake in rats.

This study was designed to determine the specificity and physiological nature of short-term satiety effects of cholecystokinin (CCK) in rats with intact and transected vagal nerves. Rats with-the gastric fistulas, closed or open, were used for normal feeding or sham feeding of liquid meal offered for 30 min. CCK-8 (0.5-10 nmol/kg) injected intraperitoneally (ip) 15 min before feeding inhibited food intake dose dependently in both normal-fed and sham-fed rats at a minimal inhibitory dose of 1 nmol/kg. CCK-8 at the same doses caused a potent stimulation of pancreatic protein secretion, reaching maximum at a dose of approximately 0.5 nmol/kg. Pretreatment with a potent CCK receptor antagonist, L-364,718 (2.5 mg/kg ip), increased food intake during normal feeding (but not sham feeding) and almost completely blocked the satiety and pancreatic stimulatory effects of CCK. When feeding was preceded by intragastric administration of proteinase inhibitor (Foy-305, 200 mg/kg), food preload, or diversion of bile-pancreatic secretion to the exterior, there was a significant increase in the plasma level of CCK and an inhibition of food intake by about 36, 78, and 25%, respectively. Pretreatment with L-364,718 completely abolished this inhibition by Foy-305 and bile-pancreatic diversion and reduced that caused by food preload. Among other gut peptides given ip (10 nmol/kg) only bombesin reduced food intake, whereas gastrin, secretin, gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), and peptide YY (PYY) were ineffective.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Role of leukotrienes and platelet activating factor in acute gastric mucosal lesions in rats.

Leukotriene C4 (LTC4) and platelet activating-factor (PAF) were found to affect gastric microcirculation and mucosal integrity but their role in acute gastric damage has not been established. The present study with rats confirms that exogenous LTC4 (10 micrograms/kg.h s.c.) or PAF (10 micrograms/kg i.p.) alone caused only mild gastric mucosal injury but greatly augmented mucosal lesions produced by other irritants such as absolute ethanol, taurocholate, aspirin or stress. These acute lesions were accompanied by a significant increase in mucosal generation of LTC4, and the addition of PAF further increased it. Pretreatment with BN 52021, a PAF receptor antagonist, abolished PAF-induced gastric lesions and reduced LTC4 generation in tests with PAF plus ethanol. Nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway, and FPL 55712, an LTC receptor-antagonist, reduced dose dependently the extent of gastric damage in various models of gastric lesions. Again, these protective effects were accompanied by a reduction in mucosal LTC4 formation. In addition, the protection induced by nordihydroguaiaretic acid was reversed in part by the pretreatment with indomethacin, suggesting that it could be attributed to increased biosynthesis of protective PG. The results indicated that LTC4 biosynthesis is increased in various forms of gastric damage and that LTC4 may be involved in the pathogenesis of this damage.

Animals↗